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.

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.

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.

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.

Poor sleep quality increases symptoms of depression and anxiety in postpartum women.

This study evaluated the relationship between sleep quality and symptoms of depression and anxiety in women studied in pregnancy and postpartum. Scores on standardized measures of sleep (PSQI) at 6 months postpartum, and symptoms of anxiety and depression (OASIS, the PHQ9, and EPDS) were assessed by structured interviews in 116 women in pregnancy and/or postpartum. Poor sleep quality was significantly associated with greater symptoms of depression and anxiety. Women who had significantly higher OASIS (anxiety) scores (ß = .530, p < .001), PHQ9 (depression) scores (ß = .496, p < .001), and EPDS (postpartum depression and anxiety) scores (ß = .585, p < .001) also had elevated total PSQI scores after adjustment for covariates, including prenatal depression and anxiety scores. Though inferences about causality are not feasible, these results support emerging research showing sleep quality is a risk factor for negative maternal affect in the postpartum period. Assessment of maternal sleep hygiene is worth consideration as a component of identifying women at risk for postpartum depression and anxiety.

Sleep Moderates and Mediates the Relationship Between Acculturation and Depressive Symptoms in Pregnant Mexican-American Women.

OBJECTIVE: Greater acculturation is associated with adverse perinatal outcomes in Mexican-American women, but the mechanisms by which acculturation influences perinatal outcomes are unclear. Pregnant acculturated Mexican-American women are more likely to engage in unhealthy prenatal behaviors relative to those less acculturated, including poor sleep. As sleep disruptions are associated with acculturation and negative perinatal outcomes, particularly maternal depression, alterations in sleep may adversely affect pregnant Mexican-American women. METHODS: Sixty pregnant women of Mexican descent completed surveys about sleep, acculturation, depressive symptoms and potential protective factor of social support. RESULTS: Acculturation, but not social support, significantly predicted increased sleep disruptions as well as overall feeling less refreshed upon waking across pregnancy. Moderation analysis indicated that more acculturated women who took longer to fall asleep reported increased depressive symptoms. Feeling refreshed upon waking also mediated the relationship between increased acculturation and elevated maternal depressive symptoms. CONCLUSIONS: Acculturation and altered sleep contribute to greater risk in Mexican-American women for maternal depressive symptoms in the perinatal period. These findings have implications for prevention and treatment of maternal mental health disorders, which may adversely affect perinatal outcomes in the vulnerable Mexican-American population.

Cerebrospinal fluid inflammatory cytokines and aggression in personality disordered subjects.

BACKGROUND: Neurochemical studies have pointed to a modulatory role in human aggression for a variety of central neurotransmitters and neuromodulators such as cytokines. While animal studies of cytokines suggest an aggression-facilitating role for central cytokines, especially for interleukin-1ß and other cytokines, no cerebrospinal fluid studies of cytokines have yet been reported in regard to human aggression. METHODS: Basal lumbar cerebrospinal fluid samples were obtained from 38 physically healthy subjects with DSM-5 Personality Disorder and assayed for cerebrospinal fluid interleukin-6 (log IL-6) and cerebrospinal fluid soluble IL-1 Receptor II protein in the context of their relationship with measures of aggression. RESULTS: Cerebrospinal fluid soluble interleukin-1 Receptor II (r=.35, r(2) = .12, P= .03), but not log interleukin-6 (r = -.05, r(2) = .00, P= .76), levels were positively correlated with a composite measure of aggression. Adding relevant covariates, including cerebrospinal fluid levels of serotonin and dopamine metabolites, to the statistical model doubled the strength of this relationship (partial r = .54, r(2) = .29, P= .002). No relationship was seen with history of suicidal behavior or with any measure of impulsivity, negative affectivity, or of general dimensions of personality. CONCLUSION: These data suggest a positive relationship between at least one inflammatory cytokine in the central nervous system and aggression in human subjects. This finding adds to the complex picture of the central neurochemistry of impulsive aggression in human subjects.

Cerebrospinal fluid and plasma C-reactive protein and aggression in personality-disordered subjects: a pilot study.

C-reactive protein (CRP), in the plasma, serves as a marker of systemic inflammation and has been shown to correlate with history of actual aggressive behavior, and as a personality trait of aggressive tendency, in human subjects. This pilot study was conducted to determine if plasma CRP levels are correlated with cerebrospinal fluid levels (CSF CRP) and if CSF CRP also correlates with aggression. If so, this would suggest a role for central inflammatory processes in human aggression. Both plasma and basal lumbar CSF samples were obtained from 17 subjects with DSM-5 personality disorder and assayed for CRP. Plasma and CSF CRP levels were correlated (r = 0.65, p = 0.005) and each correlated with aggression (Plasma: r = 0.53, p = 0.029; CSF: r = 0.84, p < 0.001). When considered simultaneously, CSF CRP, but not plasma CRP, uniquely correlated with aggression. No relationship was seen with other measures of psychopathology. These data suggest a positive relationship between central nervous system CRP and aggression in humans.

Placental corticotrophin-releasing hormone trajectories in pregnancy: Associations with postpartum depressive symptoms.

OBJECTIVE: Depressive symptoms following birth are common and can have adverse effects for mothers, children, and families. Changes in hypothalamic-pituitary-adrenal (HPA) axis regulation during pregnancy may be implicated in the development of postpartum depressive symptoms, particularly changes in placental corticotropinreleasing hormone (pCRH). However, few studies have tested how dynamic pCRH changes over pregnancy relate to postpartum depressive symptoms. This preregistered investigation tests associations of both pCRH levels and changes from early to late pregnancy with postpartum depressive symptoms. METHODS: The sample consists of 173 women studied in early, mid, and late pregnancy who later reported on depressive symptoms with the Edinburgh Postpartum Depression Scale during interviews at 1, 6 and 12 months postpartum. Blood samples were collected at each prenatal timepoint and assayed for pCRH using radioimmunoassay. Latent growth curve analysis was employed to identify distinct trajectories of pCRH during pregnancy. RESULTS: We identified three prenatal pCRH trajectories labeled as typical, flat, and accelerated. Each trajectory showed exponential increases in pCRH levels over the course of gestation but differed in overall levels and rates of change. pCRH levels were not associated with postpartum depressive symptoms. However, women with accelerated pCRH trajectories reported marginally higher depressive symptoms one month postpartum. Primary analysis models adjusted for marital status, income, prepregnancy BMI, parity, prenatal depressive symptoms, and gestational age. CONCLUSIONS: These findings add to our understanding of dynamic changes to maternal HPA axis regulation during pregnancy and contribute to growing evidence on how pCRH changes relate to the development of postpartum depressive symptoms.

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.

Maternal Early Life Adversity and Infant Stress Regulation: Intergenerational Associations and Mediation by Maternal Prenatal Mental Health.

Early life adversity is a potent risk factor for poor mental health outcomes across the lifespan, including offspring vulnerability to psychopathology. Developmentally, the prenatal period is a sensitive window in which maternal early life experiences may influence offspring outcomes and demarcates a time when expectant mothers and offspring are more susceptible to stressful and salutary influences. This prenatal plasticity constituted the focus of the current study where we tested the association of maternal early life adversity with infant stress regulation through maternal prenatal internalizing symptoms and moderation by prenatal social support. Mother-infant dyads (n = 162) were followed prospectively and mothers completed assessments of social support and depressive and anxiety symptoms across pregnancy. Infants completed standardized stress paradigms at one month and six months. There were several key findings. First, maternal prenatal depressive symptoms significantly mediated predictions of infant cortisol reactivity to the heel stick at one month from maternal early life adversity: specifically, maternal early life adversity positively predicted depressive symptoms in pregnancy, which in turn predicted dampened infant cortisol reactivity. Second, prenatal social support did not significantly moderate predictions of depressive or anxiety symptoms in pregnancy from maternal early life adversity nor did it alter the associations of maternal depressive or anxiety symptoms with infant stress regulation. These results suggest that maternal prenatal mental health is a key mechanism by which maternal early life adverse experiences affect offspring risk for psychopathology. We discuss potential clinical and health implications of dysregulated infant cortisol reactivity with respect to lifespan development.

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.

Acculturation, maternal cortisol, and birth outcomes in women of Mexican descent.

OBJECTIVE: This study investigated the effects of acculturation on cortisol, a biological correlate of maternal psychological distress, and perinatal infant outcomes, specifically gestational age at birth and birth weight. METHODS: Fifty-five pregnant women of Mexican descent were recruited from a community hospital, and their saliva samples were collected at home for 3 days during pregnancy at 15 to 18 weeks (early), 26 to 32 weeks (mid), and more than 32 weeks (late) of gestation and once in the postpartum period (4-12 weeks). These values were used to determine the diurnal cortisol slope at each phase of pregnancy. Mothers also completed an acculturation survey and gave permission for a medical chart review to obtain neonate information. RESULTS: Multiple regression analyses determined that greater acculturation levels significantly predicted earlier infant gestational age at birth (R(2) = 0.09, p = .03). Results from t tests revealed that mothers of low-birth-weight infants (<2500 g) had significantly higher acculturation scores than mothers of infants with birth weight greater than 2500 g (t = -2.95, p = .005). A blunted maternal cortisol slope during pregnancy was also correlated with low birth weight (r = -0.29, p = .05) but not gestational age (r = -0.08, p = .59). In addition, more acculturated women had a flatter diurnal cortisol slope late in pregnancy (R(2) = 0.21, p = .01). Finally, diurnal maternal cortisol rhythms were identified as a potential mediator between increased acculturation and birth weight. CONCLUSIONS: This study associated increased acculturation with perinatal outcomes in the US Mexican population. This relationship may be mediated by prenatal maternal diurnal cortisol, which can program the health of the fetus leading to several adverse perinatal outcomes.

The occurrence of preterm delivery is linked to pregnancy-specific distress and elevated inflammatory markers across gestation.

There is mounting evidence that stress during pregnancy can have detrimental effects on gestation and birth. Existing studies indicate that prenatal stress may increase levels of circulating inflammatory markers that are associated with prematurity and pregnancy complications, suggesting that stress-related changes in the cytokine milieu may increase the risk of poor pregnancy outcome. Previous studies, however, have not clearly connected stress during pregnancy to changes in inflammatory mediators and, in turn, to clinically-relevant outcomes such as premature delivery. The present study sought to directly connect prenatal stress and changes in inflammatory markers to preterm delivery and gestational age at birth (GAB). A sample of 173 women was recruited during the first trimester of pregnancy and followed through delivery. Overall stress, pregnancy-specific distress, and inflammatory markers were assessed early and later in pregnancy, and the predictive value of these measures for preterm birth and GAB was determined. There were significant differences in pregnancy-specific distress, IL-6, and TNF-α between women who delivered prematurely versus those who delivered at term, and elevated levels of pregnancy-specific distress, IL-6, and TNF-α were predictive of shortened GAB overall. Importantly, in many cases, the effects of overall stress and pregnancy-specific distress on GAB were mediated by levels of circulating inflammatory markers. Collectively, these data provide strong evidence that prenatal stress experiences can affect the timing of parturition via alterations in circulating inflammatory mediators, and underscore the need for ongoing research aimed at further understanding the mechanisms and effects of prenatal stress on maternal and infant health.

Association between diagnosed perinatal mood and anxiety disorders and adverse perinatal outcomes.

PURPOSE: To determine whether a diagnosis of a perinatal mood and anxiety disorder (PMAD) is associated with adverse perinatal outcomes. METHODS: Mental health symptom screening and diagnostic data from 82 women with single gestation in the Healthy Babies Before Birth study conducted from 2013 to 2018 were obtained by clinic interview. If a woman scored over 10 on the Patient Health Questionnaire (PHQ-9) or endorsed the suicidality item; or scored over 7 on the Overall Anxiety Severity and Impairment Scale (OASIS), a Structured Clinical Interview for DSM-IV (SCID) Axis I Disorders was administered. An adverse perinatal outcome was operationalized as a diagnosis of gestational diabetes mellitus, intrauterine growth restriction, preeclampsia, chorioamnionitis, hemorrhage, fetal death, preterm birth, or a low birthweight baby, and abstracted from the medical records. RESULTS: Women were between 22.0 and 45.0 years old (Mean age = 33.1 ± 4.3). Mean BMI was 24.7 ± 5.6 (Range 16.8 to 47.1). Nineteen percent (16) of the 82 women had a SCID diagnosis of a PMAD. Thirty-seven percent (30) had a diagnosed adverse perinatal outcome. Multiple logistic regression was conducted with these predictors: SCID diagnosis of a PMAD, maternal age, BMI. All predictors were significant with respective odds ratios as follows: OR = 3.58, 95% CI 1.03-12.44, p = .045; OR = 2.30, 95% CI 1.21-4.38, p = .011; OR = 1.69, 95% CI 1.06-2.69, p = .027. CONCLUSIONS: A PMAD diagnosis was associated with 3.5 times higher odds of having an adverse perinatal outcome. For every 5 years a woman aged or every five units her BMI increased her odds of having an adverse perinatal outcome increased. Older age and increased BMI are well established adverse perinatal outcome risk factors. These results suggest that mental illness risk should also be consistently assessed in obstetric settings.

Anxiety in pregnancy and length of gestation: Findings from the healthy babies before birth study.

OBJECTIVES: Anxiety is prevalent in pregnancy and predicts risk of adverse birth outcomes. Many instruments measure anxiety in pregnancy, some of which assess pregnancy anxiety defined as maternal concerns about a current pregnancy (e.g., baby, childbirth). The present study examined covariance among four anxiety or distress measures at two times in pregnancy and tested joint and individual effects on gestational length. We hypothesized that the common variance of the measures in each trimester would predict earlier delivery. METHOD: Research staff interviewed 196 women in first and third trimester utilizing a clinical screener of anxiety severity/impairment, two instruments measuring pregnancy anxiety, and one on prenatal distress. Birth outcomes and medical risk factors were obtained from medical records after birth. Structural equation modeling fit latent factors for each trimester from the four measures. Subsequent models tested whether the latent factors predicted gestational length, and unique effects of each measure. RESULTS: The third-trimester pregnancy anxiety latent factor predicted shorter gestational length adjusting for mother's age, education, parity, and obstetric risk. Scores on a four-item pregnancy-specific anxiety measure (PSAS) in third trimester added uniquely to prediction of gestational length. In first trimester, scores on the clinical screener (OASIS) uniquely predicted shorter gestational length whereas the latent factor did not. CONCLUSION: These results support existing evidence indicating that pregnancy anxiety is a reliable risk factor for earlier birth. Findings point to possible screening for clinically significant anxiety symptoms in the first trimester, and pregnancy-specific anxiety thereafter to advance efforts to prevent earlier delivery. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

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.

The moderating role of resilience resources in the association between stressful life events and symptoms of postpartum depression.

BACKGROUND: One in seven women experience postpartum depression, posing a serious public health concern. One of the most robust predictors of elevated postpartum depressive symptoms is major stressful life events that occur during pregnancy. Having greater resilience resources that promote successful adaptation to stressful demands may be protective in the face of stress during pregnancy. The current study tested whether three resilience resources- mastery, dispositional optimism, and spirituality- each predicted early symptoms of postpartum depression and moderated the hypothesized association between experiencing stressful life events during pregnancy and symptoms of postpartum depression. METHODS: The sample included 233 women who participated in a prospective longitudinal study from pregnancy through postpartum. Depressive symptoms were assessed at approximately 4 to 8 weeks after birth, whereas resilience resources and stressful life events were measured in pregnancy. Multiple linear regressions were used to test hypotheses. RESULTS: Stressful life events predicted greater symptoms of depression postpartum. Mastery and optimism predicted fewer symptoms of depression postpartum. Mastery moderated the association between stressful life events and symptoms of depression when controlling for previous psychiatric history, t(231) = -1.97, p=.0497. LIMITATIONS: There was some attrition among study participants across timepoints, which was accounted for in analyses with multiple imputation. CONCLUSIONS: These findings point to the protective nature of a mother's sense of mastery in the face of major life stressors during pregnancy and suggest this is an important construct to target in interventions addressing postpartum depression.

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.

Maternal prenatal anxiety trajectories and infant developmental outcomes in one-year-old offspring.

A longitudinal study of a sample of women and their offspring from two urban areas (N = 233) was conducted to test whether maternal prenatal anxiety trajectories from early to late pregnancy are associated with 12-month infant developmental outcomes, independent of maternal postpartum anxiety symptoms, prenatal and postpartum depressive symptoms, parity, birth outcomes and maternal education. Three types of maternal anxiety trajectories over the course of pregnancy were identified and labeled increasing, decreasing, and stable-low. Only increasing maternal prenatal anxiety was associated with 12-month infant outcomes, specifically lower Bayley-III scores on receptive language and gross motor skills. Maternal anxiety measured at each individual timepoint in pregnancy was not associated with infant Bayley-III outcomes, highlighting the importance of examining trajectories of maternal affect.