Prenatal mood and anxiety disorders and associated cytokine changes.

BACKGROUND: We examined whether women with prenatal mood and anxiety disorders would exhibit differential pro- and anti-inflammatory marker trajectories during the prenatal and postpartum periods compared to women without these disorders. METHODS: Approximately 179 pregnant women participated in a longitudinal study conducted in two urban areas. Blood samples for inflammatory markers were collected at six study visits. The Structured Clinical Interview for the DSM-IV (SCID) was administered to participants scoring above cutoffs on anxiety and depression. Pregnant women with SCID Axis I diagnoses of mood and/or anxiety disorders were compared to other participants on inflammatory markers. Multilevel modeling tested associations between SCID diagnoses and within-person interleukin (IL)6 and IL10 trajectories. RESULTS: Prenatal SCID diagnoses were associated with linear, quadratic and cubic change in IL6 from prenatal to postpartum timepoints. Women with a prenatal SCID diagnosis had steeper decreases and increases in IL6 during prenatal and postpartum periods. SCID diagnoses were associated with lower IL10 in mid-pregnancy to postpartum (b = -0.078, SE = 0.019; p = .015). LIMITATIONS: Future studies would benefit from a larger sample size and a larger number of participants with SCID diagnoses. Future research should also examine whether different prenatal Axis 1 diagnoses are associated with different patterns of immune response in pregnancy. CONCLUSIONS: Pregnant women with prenatal mood and anxiety disorders had greater fluctuations in IL6 across prenatal and postpartum periods and lower IL10 through pregnancy and postpartum. They may have different proinflammatory states that remain after birth without a reciprocal anti-inflammatory response.

Mothers' and Children's Mental Distress and Family Strain during the COVID-19 Pandemic: A Prospective Cohort Study.

BACKGROUND: The COVID-19 pandemic had a widespread impact on families with dependent children. To better understand the impact of the pandemic on families' health and relationships, we examined the association between mothers' and children's mental distress and family strain. METHODS: Three waves of the COVID-19 Impact Survey were analyzed, collected from a subsample of mother-child pairs (n = 157) from the Alberta Pregnancy Outcomes and Nutrition (APrON) longitudinal cohort in Alberta, Canada. Latent class analyses were performed to determine patterns and group memberships in mothers' and children's mental distress and family strain. Multivariable logistic regression models were conducted to test associations between mothers' and children's mental distress and family strain trajectory classes. RESULTS: Mothers with medium/high levels of mental distress were at increased odds of experiencing high family strain compared to those with low levels of distress (medium aOR = 3.90 [95% CI: 1.08-14.03]; high aOR = 4.57 [95% CI: 1.03-20.25]). The association between children's mental distress and family strain was not significant (aOR = 1.75 [95% CI: 0.56-5.20]). CONCLUSION: Mothers' mental distress, but not children's, was associated with family strain during the pandemic. More distressed individuals experienced greater family strain over time, suggesting that this association may become a chronic problem.

Partner relationship quality and IL-6:IL-10 trajectories from pregnancy to a year after-birth.

BACKGROUND: Inflammatory activity during pregnancy and the postpartum period shifts systematically due to pregnancy progression, delivery, and postpartum recovery. Factors that deregulate inflammatory activity increase the risk for adverse pregnancy outcomes and slower postpartum recovery. The IL-6:IL-10 or TNF-α:IL-10 ratio is potentially one way to capture peripheral inflammatory regulation; higher values indicate that anti-inflammatory IL-10 is less effective at regulating pro-inflammatory TNF-α or IL-6, skewing towards maladaptive pro-inflammatory profiles. Associations between partner relationship quality and IL-6:IL-10 or TNF-α:IL-10 trajectories during pregnancy and the postpartum period have not been assessed. The purpose of this study was to test whether partner relationship quality (support, conflict) is associated with attenuated IL-6, IL-10, TNF-α, TNF-α:IL-10 or IL-6:IL-10 trajectories from the third trimester to the postpartum period. METHODS: A sample of 162 women from the Healthy Babies Before Birth study reported on partner relationship quality (support and conflict) using the Social Support Effectiveness Questionnaire during the third trimester. Plasma samples were collected in the third trimester and at 1-, 6- and 12-months postpartum, and assayed for TNF-α, IL-6 and IL-10. Associations between both indicators of relationship quality (support and conflict) and TNF-α, IL-6, IL-10, IL-6:IL-10, TNF-α:IL-10 trajectories were tested using multi-level modelling, controlling for sociodemographic, pregnancy and health variables. RESULTS: Partner support interacted with time to predict IL-6:IL-10 trajectories, linear: b = -0.176, SE = 0.067, p =.010, quadratic: b = 0.012, SE = 0.005, p =.009. Lower partner support was associated with steeper increases in IL-6:IL-10 from the third trimester to 6 months postpartum, followed by steeper decreases in IL-6:IL-10 from 6 months postpartum to a year after birth. Partner conflict was not associated with IL-6:IL-10 levels at study entry, b = 0.233, SE = 0.219, p =.290, or over time, p's > 0.782. Neither indicator of partner relationship quality was associated with TNF-α, IL-6, IL-10, or TNF-α:IL-10 trajectories, p's > 0.205. CONCLUSION: Lower partner support may be associated with reduced moderation of IL-6 by IL-10 between pregnancy and a year postpartum, with possible consequences for maternal health and well-being.

Pregnancy-specific anxiety and gestational length: The mediating role of diurnal cortisol indices.

BACKGROUND: Preterm birth or shorter gestation is a common adverse pregnancy outcome. Pregnancy-specific anxiety is robustly associated with risk for shorter gestation. Hypothalamic-pituitary-adrenal (HPA) dysregulation, indicated by diurnal cortisol index variability [slope, area-under-the-curve (AUC) or cortisol awakening response (CAR)], could mediate associations between pregnancy-specific anxiety and shorter gestation. The purpose of this study was to explore whether diurnal cortisol index variability mediates associations between pregnancy-specific anxiety and gestational length. METHODS: A sample of 149 women from the Healthy Babies Before Birth study reported pregnancy-specific anxiety in early pregnancy. Saliva samples were taken at three times during pregnancy, for two days each, at wake, 30 min post wake, noon, and evening. Diurnal cortisol indices were calculated using standard approaches. Pregnancy cortisol index variability was calculated across pregnancy timepoints. Gestational length was derived from medical charts. Covariates were sociodemographics, parity and obstetric risk. Mediation models were tested using SPSS PROCESS. RESULTS: There was a significant indirect effect of pregnancy-specific anxiety on gestational length via CAR variability, b(SE)= -0.102(0.057), .95CI [- 0.227,- 0.008]. Higher pregnancy-specific anxiety was associated with lower CAR variability, b(SE)= -0.019(0.008), p = .022, and lower CAR variability was associated with shorter gestation, b(SE)= 5.29(2.64), p = .047. Neither AUC or slope variability mediated associations between pregnancy-specific anxiety and gestational length. CONCLUSION: Lower CAR variability during pregnancy mediated the association between higher pregnancy-specific anxiety and shorter gestational length. Pregnancy-specific anxiety could dysregulate HPA axis activity, as indicated by lower CAR variability, demonstrating the importance of the HPA axis system in regulating pregnancy outcomes.

Maternal anxiety, depression and stress affects offspring gut microbiome diversity and bifidobacterial abundances.

Uncovering mechanisms underlying fetal programming during pregnancy is of critical importance. Atypical neurodevelopment during the pre- and immediate postnatal period has been associated with long-term adverse health outcomes, including mood disorders and aberrant cognitive ability in offspring. Maternal factors that have been implicated in anomalous offspring development include maternal inflammation and tress, anxiety, and depression. One potential mechanism through which these factors perturb normal offspring postnatal development is through microbiome disruption. The mother is a primary source of early postnatal microbiome seeding for the offspring, and the transference of a healthy microbiome is key in normal neurodevelopment. Since psychological stress, mood disorders, and inflammation have all been implicated in altering maternal microbiome community structure, passing on aberrant microbial communities to the offspring that may then affect developmental outcomes. Therefore, we examined how maternal stress, anxiety and depression assessed with standardized instruments, and maternal inflammatory cytokine levels in the pre- and postnatal period are associated with the offspring microbiome within the first 13 months of life, utilizing full length 16S sequencing on infant stool samples, that allowed for species-level resolution. Results revealed that infants of mothers who reported higher anxiety and perceived stress had reduced alpha diversity. Additionally, the relative taxonomic quantitative abundances of Bifidobacterium dentium and other species that have been associated with either modulation of the gut-brain axis, or other beneficial health outcomes, were reduced in the offspring of mothers with higher anxiety, perceived stress, and depression. We also found associations between bifidobacteria and prenatal maternal pro-inflammatory cytokines IL-6, IL-8, and IL-10. In summary, specific microbial taxa involved in maintaining proper brain and immune function are lower in offspring born to mothers with anxiety, depression, or stress, providing strong evidence for a mechanism by which maternal factors may affect offspring health through microbiota dysregulation.

Maternal early life stress is associated with pro-inflammatory processes during pregnancy.

Early life stress (ELS) is common in the United States and worldwide, and contributes to the development of psychopathology in individuals with these experiences and their offspring. A growing body of research suggests that early life stress may contribute to adverse health partly through modulation of immune (and particularly inflammatory) responses. Therefore, increased maternal prenatal inflammation has been proposed as a mechanistic pathway by which the observed cross-generational effects of parental early life stress on child neuropsychiatric outcomes may be exerted. We examined associations between early life stress and molecular markers of inflammation (specifically pro-inflammatory gene expression and receptor-mediated transcription factor activity) and a commonly studied circulating marker of inflammation (C-Reactive Protein) in a diverse group of women in or near their third trimester of pregnancy, covarying for age, race/ethnicity, BMI, concurrent infection, concurrent perceived stress, and per capita household income. Mothers who experienced higher levels of early life stress had significantly increased pro-inflammatory (NF-κB) and decreased anti-viral (IRF) transcription factor activity. Transcripts that were up or down regulated in mothers with high ELS were preferentially derived from both CD16+ and CD16- monocytes. Early life stress was not associated with elevated CRP. Taken together, these findings provide preliminary evidence for an association between ELS and a pro-inflammatory transcriptional phenotype during pregnancy that may serve as a mechanistic pathway for cross-generational transmission of the effects of early life stress on mental and physical health.

Health psychology and behavioral medicine researchers in Canada: An environmental scan.

The purpose of this study is to characterize contemporary Canadian health psychology through an environmental scan by identifying faculty, research productivity and strengths, and collaborator interconnectivity. Profiles at Canadian universities were reviewed for faculty with psychology doctorates and health psychology research programs. Publications were obtained through Google Scholar and PubMed (Jan/18-Mar/21). A total of 284 faculty were identified. Cancer, pain, and sleep were key research topics. The collaborator network analysis revealed that most were linked through a common network, with clusters organized around geography, topic, and trainee relationships. Canada is a unique and productive contributor to health psychology.

Increases in maternal depressive symptoms during pregnancy and infant cortisol reactivity: Mediation by placental corticotropin-releasing hormone.

BACKGROUND: Maternal depressive symptoms in pregnancy may affect offspring health through prenatal programming of the hypothalamic-pituitary-adrenal (HPA) axis. The biological mechanisms that explain the associations between maternal prenatal depressive symptoms and offspring HPA axis regulation are not yet clear. This pre-registered investigation examines whether patterns of maternal depressive symptoms in pregnancy are associated with infant cortisol reactivity and whether this association is mediated by changes in placental corticotropin-releasing hormone (pCRH). METHOD: A sample of 174 pregnant women completed assessments in early, mid, and late pregnancy that included standardized measures of depressive symptoms and blood samples for pCRH. Infant cortisol reactivity was assessed at 1 and 6 months of age. RESULTS: Greater increases in maternal depressive symptoms in pregnancy were associated with higher cortisol infant cortisol reactivity at 1 and 6 months. Greater increases in maternal depressive symptoms in pregnancy were associated with greater increases in pCRH from early to late pregnancy which in turn were associated with higher infant cortisol reactivity. CONCLUSIONS: Increases in maternal depressive symptoms and pCRH over pregnancy may contribute to higher infant cortisol reactivity. These findings help to elucidate the prenatal biopsychosocial processes contributing to offspring HPA axis regulation early in development.

Impact of the COVID-19 Pandemic on Canadian Social Connections: A Thematic Analysis.

Background: On March 11, 2020, the World Health Organization declared COVID-19 a worldwide pandemic. Responses to the pandemic response disrupted Canadian social connections in complex ways; because social connections are determinants of health and well-being, their disruption could adversely affect health and well-being. Moreover, understanding how pandemics and public health responses affect social connections could inform pandemic recovery strategy and public health approaches designed for future pandemics. The purpose of this study is to understand experiences of pandemic impact on social connections over the pandemic. Methods: A sample of 343 Canadian adults was recruited through Athabasca University and social media. Participants were predominantly White (81%) and female (88%). After the pandemic onset, participants responded to open-ended questions about the impact of the pandemic on and any changes to social connections at three time points (baseline, and three- and 6 months from study entry). Responses were categorized into epochs by date (April-June 2020 [Spring]; July-August 2020 [Summer]; September 2020-January 2021 [Fall/Winter]). Qualitative thematic analysis was used to code themes for each epoch. Results: Negative impact of the pandemic (37-45%), loss of social connections (32-36%), and alternative means of connection (26-32%) were prominent themes across the epochs. Restrictions to face-to-face connections were largest in spring (9%) and lowest in the Summer (4%). Conversely, participants increasingly reported limited contact or communication into the Fall and Winter (6-12%) as pandemic restrictions in Canada were reinstated. Conclusions: The COVID-19 pandemic threatens social connections, with negative impacts that fluctuated with COVID-19 case rates and subsequent pandemic restrictions. These findings could be used to identify targets for social supports during the pandemic recovery, and to adjust public health strategies for future pandemics that minimize impact on social connections.

Study protocol for Attachment & Child Health (ATTACHTM) program: promoting vulnerable Children's health at scale.

BACKGROUND: Children's exposure to toxic stress (e.g., parental depression, violence, poverty) predicts developmental and physical health problems resulting in health care system burden. Supporting parents to develop parenting skills can buffer the effects of toxic stress, leading to healthier outcomes for those children. Parenting interventions that focus on promoting parental reflective function (RF), i.e., parents' capacity for insight into their child's and their own thoughts, feelings, and mental states, may understand help reduce societal health inequities stemming from childhood stress exposures. The Attachment and Child Health (ATTACHTM) program has been implemented and tested in seven rapid-cycling pilot studies (n = 64) and found to significantly improve parents' RF in the domains of attachment, parenting quality, immune function, and children's cognitive and motor development. The purpose of the study is to conduct an effectiveness-implementation hybrid (EIH) Type II study of ATTACHTM to assess its impacts in naturalistic, real-world settings delivered by community agencies rather than researchers under more controlled conditions. METHODS: The study is comprised of a quantitative pre/post-test quasi-experimental evaluation of the ATTACHTM program, and a qualitative examination of implementation feasibility using thematic analysis via Normalization Process Theory (NPT). We will work with 100 families and their children (birth to 36-months-old). Study outcomes include: the Parent Child Interaction Teaching Scale to assess parent-child interaction; the Parental Reflective Function and Reflective Function Questionnaires to assess RF; and the Ages and Stages Questionnaire - 3rd edition to examine child development, all administered pre-, post-, and 3-month-delayed post-assessment. Blood samples will be collected pre- and post- assessment to assess immune biomarkers. Further, we will conduct one-on-one interviews with study participants, health and social service providers, and administrators (total n = 60) from each collaborating agency, using NPT to explore perceptions and experiences of intervention uptake, the fidelity assessment tool and e-learning training as well as the benefits, barriers, and challenges to ATTACHTM implementation. DISCUSSION: The proposed study will assess effectiveness and implementation to help understand the delivery of ATTACHTM in community agencies. TRIAL REGISTRATION: Name of registry: https://clinicaltrials.gov/. REGISTRATION NUMBER: NCT04853888 . Date of registration: April 22, 2021.

Pregnancy anxiety, placental corticotropin-releasing hormone and length of gestation.

OBJECTIVE: High pregnancy anxiety is a consistent predictor of earlier labor and delivery. Placental corticotropin-releasing hormone (pCRH) predicts earlier delivery consistently and it has been identified as a biological mediator of the association between pregnancy anxiety and gestational length. However, studies have not examined whether changes in pregnancy anxiety are associated with earlier birth as mediated by changes in pCRH during pregnancy. Accordingly, this study tests whether linear changes in pregnancy anxiety are associated with length of gestation indirectly through nonlinear increases in pCRH over pregnancy. METHODS: A sample of pregnant women (n=233) completed prenatal assessments in early pregnancy, second trimester, and third trimester that included a 4-item assessment of pregnancy anxiety and collection of blood samples assayed for pCRH using radioimmunoassay. Length of gestation was abstracted from medical records after birth. RESULTS: Increases in pregnancy anxiety from early pregnancy to third trimester predicted shorted length of gestation, as did nonlinear increases in pCRH over pregnancy. However, there was no evidence of an indirect effect of changes in pregnancy anxiety on length of gestation via changes in pCRH. CONCLUSIONS: These results indicate that linear changes in pregnancy anxiety and nonlinear changes in pCRH during pregnancy are independent risk factors for shortened gestational length. This study adds to a small but growing body of work on biopsychological processes in pregnancy and length of gestation. Modeling changes in psychological and biological processes during pregnancy could provide more insight into understanding risk for adverse pregnancy outcomes.

Inflammatory and immune marker trajectories from pregnancy to one-year post-birth.

BACKGROUND: Pregnancy is an immunomodulatory state, with reported systematic changes in inflammatory and immune activity by pregnancy stage. Published data are inconsistent as to how inflammatory and immune markers change and recover across pregnancy and the postpartum period, or the sociodemographic, health and pregnancy-related factors that could affect biomarker trajectories. The purpose of this study is to describe inflammatory and immune marker trajectories from pregnancy to a year post-birth, and to test associations with sociodemographic, health and pregnancy-related variables. METHODS: A sample of 179 pregnant women were assessed three times during pregnancy (between 8 and 36 weeks gestation) and three times during the postpartum period (between 1 and 12 months). Maternal sociodemographic characteristics, health, and pregnancy factors were obtained at study entry. Blood samples from each assessment were assayed for interleukin(IL)-6, tumor necrosis factor(TNF)α, IL-8, IL-10, and interferon(IFN)γ. Multilevel modelling was used to characterize biomarker trajectories and associations with sociodemographic and health variables. RESULTS: Distinct trajectories over time emerged for each biomarker. Male pregnancies were associated with higher TNFα, IL-10, and IFNγ; higher pre-pregnancy BMI was associated with higher IL-6 and IFNγ. Nulliparity was associated with greater increases in IL-6 and TNFα. CONCLUSIONS: Patterns observed for inflammatory and immune markers from pregnancy to a year postpartum support the hypothesis that the maternal immune system changes systematically across pregnancy and through an extended postpartum period. Parity, pre-pregnancy BMI and child sex are associated with inflammatory marker patterns over time. These results contribute to our understanding of how immune system activity changes from pregnancy to the post-birth period, and the factors that could affect those changes.

The ATTACH™ program and immune cell gene expression profiles in mothers and children: A pilot randomized controlled trial.

BACKGROUND: Children exposed to adversity and toxic stress are at increased risk for poor health across the lifespan, possibly through alterations to immune pathways. Parenting interventions could buffer the effect of adversity on child immune activity. The purpose of this study was to test whether mothers and children who were randomly assigned to a parenting intervention (ATTACH™) had healthier post-intervention immune cell gene expression patterns, as indexed by the Conserved Transcriptional Response to Adversity (CTRA), compared with mothers and children in a wait-list control group. METHODS: A sample of 20 mother-child dyads were recruited from a domestic violence shelter in Calgary, AB, Canada. The ATTACH™ program is a 10-week psycho-educational intervention that fosters maternal reflective function, i.e. how to understand and respond to mental states. Dyads were randomly assigned to an intervention or wait-list group. Dried blood spots were collected from both groups post-intervention, subjected to RNA sequencing, and assessed for CTRA gene expression using mixed effect linear model analysis. Covariates were age, child sex, maternal race/ethnicity, and maternal medication use. RESULTS: In unadjusted models, differences by treatment group were detected, F(1,1794) â€‹= â€‹4.26, p â€‹= â€‹.039. Mothers and children who completed the ATTACH™ intervention had lower CTRA scores, indicating healthier immune cell gene expression profiles (Mn â€‹= â€‹-0.36, SE â€‹= â€‹0.17), compared with mothers and children in the wait-list control group (Mn â€‹= â€‹0.11, SE â€‹= â€‹0.15). Results persisted after controlling for covariates. DISCUSSION: ATTACH™ participation predicted healthier immune cell gene expression profiles post-intervention compared with wait-list controls. Parenting interventions could decrease the impact of toxic stress on maternal-child immune health.

Cross-Sectional Study Protocol for the COVID-19 Impact Survey of Mothers and Their 7-11 Year Old Children in Alberta, Canada.

Objectives: Our aim is to understand the effect of the COVID-19 pandemic on families who have been followed longitudinally in two cohorts studied in Alberta, Canada. We will examine household infections during the COVID-19 pandemic, financial impact, domestic violence, substance use, child school and daily life and relationships in the home. We will identify risk and protective factors for maternal mental health outcomes using longitudinal data that can inform policy and government resource allocation in future disasters. Methods: Mothers who are currently participating in two longitudinal studies, Alberta Pregnancy Outcomes and Nutrition (APrON; N = 1,800) and All Our Families (AOF: N = 2,534) were eligible to participate. Mothers were invited to complete the baseline COVID-19 Impact Survey (20-30 min) within 4 months of March 15, 2020, which was when the province of Alberta, Canada, implemented school closures and physical-distancing measures to prevent the spread of COVID-19. Mothers were asked to report on their own, their child's and their family's functioning. Mothers were re-surveyed at 6 months after completion of the initial COVID-19 Impact Survey, and will be re-surveyed again at 12 months. Results: Responses from participants in both cohorts will be examined in harmonized analyses as well as separately. Descriptive, multivariable analysis will be undertaken to examine risk and resiliency over time and factors that predict mental health and well-being. Conclusions: This study will provide timely information on the impact of COVID-19 for Albertan families. It will identify risk and protective factors for mental health and well-being among contemporary urban families supported by a publicly funded health care system to inform allocation of resources to support those most vulnerable during a global pandemic.

Socioeconomic status, diabetes, and gestation length in Native American and White women.

OBJECTIVE: "Diminishing returns" of socioeconomic status (SES) suggests that higher SES may not confer equivalent health benefits for ethnic minority individuals as compared to White individuals. Little research has tested whether diminishing returns also affects Native Americans. The objective of this study was to determine whether higher SES is associated with lower diabetes risk and longer gestational length in both Native American and White women, and whether SES predicts gestational length indirectly via diabetes risk. METHOD: A sample of 674,014 Native American and White women was drawn from a population-based California cohort of singleton births (2007-2012). Education, public health insurance status, gestational length, and diabetes diagnosis were extracted from a state-maintained birth cohort database. Covariates were age, health behaviors, pregnancy variables, residence rurality, and prepregnancy body mass index. RESULTS: In logistic regression models, the race by SES interaction (both education and insurance status) was associated with diabetes risk. Compared to high-SES White women, high- and low-SES Native American women had highest and equivalent diabetes risk. In path analyses, the race by SES interaction indirectly predicted gestational length through diabetes, ps < .001. For White women, an indirect effect of diabetes was detected, ps < .001, such that higher SES was associated with reduced risk for diabetes and thus longer gestational length. For Native American women, no indirect effect was detected, ps > .067. CONCLUSIONS: Among Native American women, higher SES did not confer protection against diabetes or shorter gestational length. These findings are consistent with the diminishing returns of SES phenomenon. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Postpartum sleep loss and accelerated epigenetic aging.

BACKGROUND: Insufficient sleep has been linked to accelerated biological aging in adults, providing a possible mechanism through which sleep may influence disease risk. In the current paper, we test the hypothesis that short sleep in postpartum would predict older biological age in women one year post birth, as indicated by accelerated epigenetic aging. METHODS: As part of a larger study of pregnancy and postpartum health (Healthy Babies Before Birth, HB3), 33 mothers provided blood samples for epigenetic aging clock estimates. intrinsic epigenetic age acceleration (IEAA), extrinsic apigenetic age acceleration, phenotypic epigenetic age acceleration (PEAA), GrimAge, DNAmPAI-1, and DNAm telomere length (TL) were calculated using established protocols. Sleep duration was categorized as insufficient sleep (<7 hours per night) or healthy sleep duration (7+ hours per night). Sleep quality was determined using the Pittsburgh Sleep Quality Index (Global score >5). RESULTS: Maternal postpartum sleep duration at 6 months, but not 12 months, following a birth was predictive of older 12-month IEAA, B (SE) = 3.0 (1.2), P = .02, PEAA, B (SE) = 7.3 (2.0), P = .002, and DNAmTL, B (SE) = -0.18 (0.07), P = .01, but not other indices, all P> .127. Self-reported poor sleep quality at 6 and 12 months was not significantly related to epigenetic age. CONCLUSIONS: These findings suggest that insufficient sleep duration during the early postpartum period is associated with accelerated biological aging. As the sample size is small, additional research is warranted with a larger sample size to replicate these findings.

Prenatal maternal distress and immune cell epigenetic profiles at 3-months of age.

BACKGROUND: Prenatal maternal distress predicts altered offspring immune outcomes, potentially via altered epigenetics. The role of different kinds of prenatal maternal distress on DNA methylation profiles is not understood. METHODS: A sample of 117 women (APrON cohort) were followed from pregnancy to the postpartum period. Maternal distress (depressive symptoms, pregnancy-specific anxiety, stressful life events) were assessed mid-pregnancy, late-pregnancy, and 3-months postpartum. DNA methylation profiles were obtained from 3-month-old blood samples. Principal component analysis identified two epigenetic components, characterized as Immune Signaling and DNA Transcription through gene network analysis. Covariates were maternal demographics, pre-pregnancy body mass index, child sex, birth gestational age, and postpartum maternal distress. Penalized regression (LASSO) models were used. RESULTS: Late-pregnancy stressful life events, b = 0.006, early-pregnancy depressive symptoms, b = 0.027, late-pregnancy depressive symptoms, b = 0.014, and pregnancy-specific anxiety during late pregnancy, b = -0.631, were predictive of the Immune Signaling component, suggesting that these aspects of maternal distress could affect methylation in offspring immune signaling pathways. Only early-pregnancy depressive symptoms was predictive of the DNA Transcription component, b = -0.0004, suggesting that this aspect of maternal distress is implicated in methylation of offspring DNA transcription pathways. CONCLUSIONS: Exposure timing and kind of prenatal maternal distress could matter in the prediction of infant immune epigenetic profiles.

Newborn metabolic vulnerability profile identifies preterm infants at risk for mortality and morbidity.

BACKGROUND: Identifying preterm infants at risk for mortality or major morbidity traditionally relies on gestational age, birth weight, and other clinical characteristics that offer underwhelming utility. We sought to determine whether a newborn metabolic vulnerability profile at birth can be used to evaluate risk for neonatal mortality and major morbidity in preterm infants. METHODS: This was a population-based retrospective cohort study of preterm infants born between 2005 and 2011 in California. We created a newborn metabolic vulnerability profile wherein maternal/infant characteristics along with routine newborn screening metabolites were evaluated for their association with neonatal mortality or major morbidity. RESULTS: Nine thousand six hundred and thirty-nine (9.2%) preterm infants experienced mortality or at least one complication. Six characteristics and 19 metabolites were included in the final metabolic vulnerability model. The model demonstrated exceptional performance for the composite outcome of mortality or any major morbidity (AUC 0.923 (95% CI: 0.917-0.929). Performance was maintained across mortality and morbidity subgroups (AUCs 0.893-0.979). CONCLUSIONS: Metabolites measured as part of routine newborn screening can be used to create a metabolic vulnerability profile. These findings lay the foundation for targeted clinical monitoring and further investigation of biological pathways that may increase the risk of neonatal death or major complications in infants born preterm. IMPACT: We built a newborn metabolic vulnerability profile that could identify preterm infants at risk for major morbidity and mortality. Identifying high-risk infants by this method is novel to the field and outperforms models currently in use that rely primarily on infant characteristics. Utilizing the newborn metabolic vulnerability profile for precision clinical monitoring and targeted investigation of etiologic pathways could lead to reductions in the incidence and severity of major morbidities associated with preterm birth.

Perinatal Maternal Anxiety and Depressive Symptoms and Child Executive Function and Attention at Two-years of Age.

The objective was to investigate whether perinatal maternal anxiety and depressive symptoms predicted child attention and executive function (EF). Mothers (N = 614) reported pregnancy and three-months postnatal anxiety and depressive symptoms. Attention and EF were measured at two-years-of-age. Covariates were demographics, alcohol use, mood disorder history, and pregnancy factors. Higher prenatal anxiety, b(SE) =.020(.005), p<.001, and postnatal depressive symptoms, b(SE) =.009(.004), p=.04, predicted poorer child attention. A prenatal-by-postnatal depressive symptom interaction emerged, b(SE) = -.005(.003), p=.04: When pregnancy depressive symptoms were low, higher postnatal symptoms predicted poorer attention. No distress variables predicted EF, p's>.22. Perinatal distress timing, kind, and change were important for child attention.