Publications by authors named "Dunkel-Schetter C"

Article Synopsis
  • Dysregulation of the HPA axis due to chronic stress during pregnancy and parenthood can negatively affect the health of parents and children.
  • Hair cortisol concentration (HCC) is a useful long-term indicator of cortisol levels, reflecting chronic stress over several months as opposed to shorter assessments.
  • Two longitudinal studies found that higher chronic stress is linked to increased HCC in pregnant women and mothers, revealing that different stressors (like work, family demands, and discrimination) can uniquely affect cortisol levels during the perinatal period and postpartum.
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Fetal exposure to prenatal stress can increase risk for psychopathology but postnatal caregiving may offset risk. This study tests whether maternal sensitivity and the home environment during early childhood modify associations of prenatal stress with offspring behavior in a sample of 127 mother-child pairs ( = 127). Mothers reported on perceived stress during pregnancy.

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Although maternal stress during pregnancy and even before conception shapes offspring risk for mental health problems, relatively little is known about the mechanisms through which these associations operate. In theory, preconception and prenatal stress may affect offspring mental health by influencing child responses to postnatal caregiving. To address this knowledge gap, this study had two aims.

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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.

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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.

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Objective: Parental trauma exposure and trauma-related distress can increase the risk of adverse health outcomes in offspring, but the pathways implicated in intergenerational transmission are not fully explicated. Accelerated biological aging may be one mechanism underlying less favorable health in trauma-exposed individuals and their offspring. This study examines the associations of preconception maternal and paternal posttraumatic stress disorder (PTSD) symptoms with child telomere length, and maternal prenatal C-reactive protein (CRP) as a biological mechanism.

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Resilience resources refer to factors that protect against the physical and mental health effects of stress exposure. This study used a cross-sectional design to test whether three individual-level resilience resources-mastery, self-esteem, and perceived social support-moderated associations between prenatal major life stressors and postpartum depressive symptoms at approximately 8 weeks postpartum. Participants were 2510 low- and middle-income women enrolled after the birth of a baby in a multi-site study of five communities in the United States.

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Objective: Exposure therapy is the frontline treatment for anxiety among adults but is underutilized during pregnancy. We qualitatively assess the prospective acceptability of exposure therapy among pregnant Latinas with elevated anxiety, a group that experiences mental health disparities.

Method: Pregnant Latinas ( = 25) with elevated anxiety were interviewed regarding their acceptability of exposure therapy following the receipt of an informational clinical video vignette.

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Background: Stress before conception and during pregnancy is associated with less favorable maternal and child health. Alterations in prenatal cortisol levels may serve as a central biological pathway linking stress to adverse maternal and child health. Research examining associations between maternal stress from childhood through pregnancy and prenatal cortisol has not been comprehensively reviewed.

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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.

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The childhood family environment can influence long-term well-being in part by modifying how individuals' respond to and cope with stress across the life span. Theoretical models propose that childhood stress will either exacerbate ) or attenuate () the effects of adult stress on mental health. This study tests whether childhood family stress modifies the association between stressful life events and depressive symptoms in pregnancy and consecutive postpartum periods.

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Article Synopsis
  • * The study found that maternal prenatal depressive symptoms serve as a key mediator between early life adversity and infants’ stress regulation, specifically affecting their cortisol levels after stress exposure at one month old.
  • * Prenatal social support did not significantly impact the relationship between a mother's early life experiences and her mental health symptoms during pregnancy, suggesting that focusing on maternal mental health is crucial for understanding and mitigating risks for infant psychopathology.
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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.

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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.

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Objectives: Anxiety is prevalent in pregnancy and predicts risk of adverse birth outcomes. Many instruments measure anxiety in pregnancy, some of which assess defined as maternal concerns about a current pregnancy (e.g.

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Background: Experiences of discrimination on the basis of race, ethnicity, and other characteristics are associated with adverse health outcomes, including elevated rates of morbidity in later life and earlier mortality. Acceleration of biological aging is a plausible pathway linking discrimination to disease risk. The objective of this study was to examine the relationship of self-reported lifetime and everyday discrimination to women's telomere length several years after birth of a child in a longitudinal cohort study.

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Article Synopsis
  • Maternal depression during pregnancy can affect how a baby's body responds to stress, specifically their cortisol levels.
  • The study looked at 174 pregnant women and found that as their depression increased during pregnancy, their babies showed higher cortisol reactivity at 1 and 6 months old.
  • It was also discovered that increased depression in mothers led to higher levels of a hormone related to stress (pCRH), which was linked to the babies' stress responses.
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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.

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Background: Two theoretical frameworks, the cumulative stress and match-mismatch model, propose that patterns of maternal depressive symptoms over early periods of offspring development predict outcomes in opposing ways. Studies have yet to test these theories across the preconception, prenatal, and early postnatal period. Study 1 identified trajectories of maternal depressive symptoms from preconception to postpartum.

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Anxiety symptoms are common among pregnant women worldwide. In the United States, prenatal anxiety symptoms tend to be elevated among Black and Latin American women as compared to non-Latina White women. Despite the high prevalence of anxiety and associations with adverse maternal and offspring outcomes, interventions have not been developed or tailored sufficiently to Black women or Latinas who need efficacious treatment.

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The developmental origins of psychopathology begin before birth and perhaps even prior to conception. Understanding the intergenerational transmission of psychopathological risk is critical to identify sensitive windows for prevention and early intervention. Prior research demonstrates that maternal trauma history, typically assessed retrospectively, has adverse consequences for child socioemotional development.

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Objective: Subjective social status (SSS) refers to an individual's perception of relative social rank. We tested associations between SSS and allostatic load, a multisystem index of physiological dysregulation, in a sample of women 1 year after the birth of a child.

Method: Participants (n = 1,168) in the Community Child Health Network study were recruited in five sites across the United States shortly after the birth of a child.

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Objective: Few studies have tested cognitive behavioral therapy to reduce prenatal anxiety despite substantial empirical support among individuals seeking treatment for anxiety symptoms. We examined whether a brief cognitive behavioral intervention delivered to low-income pregnant women would be efficacious for reducing prenatal anxiety.

Method: A sample of 100 primarily ethnic and racial minority pregnant women with subclinical anxiety (74% Latina, 18% Black; = 26.

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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.

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