Prenatal Maternal Stress and Pediatric Asthma Across Development: Adolescent Female-Specific Vulnerability.

Prenatal maternal stress (PNMS) is linked to physical sequelae in offspring, including childhood asthma. This study sought to examine the roles of objective and subjective PNMS in the development of asthma at offspring ages 5 and 15. The sample included 815 mother-child dyads from the Mater Misericordiae Mothers' Hospital-University of Queensland Study of Pregnancy. PNMS was measured via retrospective self-report during pregnancy and 3-5 days after birth. Postnatal maternal stress was measured at offspring age 5. Objective PNMS was associated with elevated asthma risk at age 5 (OR 1.21, 95% CI 1.00, 1.45, p = 0.05), albeit not above concurrent postnatal stress. Sex moderated the association between PNMS and asthma at age 15, controlling for postnatal stress. Sex stratified analyses revealed a positive association between objective PNMS and age 15 asthma in females, but not males. Results provide evidence that PNMS may impact asthma outcomes in adolescence.

Environmental Risk Factors and Cognitive Outcomes in Psychosis: Pre-, Perinatal, and Early Life Adversity.

Risk for psychosis begins to accumulate as early as the fetal period through exposure to obstetric complications like fetal hypoxia, maternal stress, and prenatal infection. Stressors in the postnatal period, such as childhood trauma, peer victimization, and neighborhood-level adversity, further increase susceptibility for psychosis. Cognitive difficulties are among the first symptoms to emerge in individuals who go on to develop a psychotic disorder. We review the relationship between pre-, perinatal, and early childhood adversities and cognitive outcomes in individuals with psychosis. Current evidence shows that the aforementioned environmental risk factors may be linked to lower overall intelligence and executive dysfunction, beginning in the premorbid period and persisting into adulthood in individuals with psychosis. It is likely that early life stress contributes to cognitive difficulties in psychosis through dysregulation of the body's response to stress, causing changes such as increased cortisol levels and chronic immune activation, which can negatively impact neurodevelopment. Intersectional aspects of identity (e.g., sex/gender, race/ethnicity), as well as gene-environment interactions, likely inform the developmental cascade to cognitive difficulties throughout the course of psychotic disorders and are reviewed below. Prospective studies of birth cohorts will serve to further clarify the relationship between early-life environmental risk factors and cognitive outcomes in the developmental course of psychotic disorders. Specific methodological recommendations are provided for future research.

Intergenerational Impacts of Maternal Stress on Early Childhood Atopy in Black Americans.

OBJECTIVE: Black children are disproportionately affected by atopic diseases (i.e., atopic dermatitis, allergic rhinitis, asthma, and food allergies), with health disparities present in early life. Studies in White samples suggest that maternal stress confers risk for offspring atopy, yet little is known about these relationships in Black populations. This study seeks to (a) examine the relationship between self-reported and physiological indicators of maternal stress and offspring atopy and (b) explore warm and responsive caregiving as a potential protective factor in Black Americans. METHODS: A sample of 179 Black mother-child dyads of varying socioeconomic status participated in a prospective longitudinal study. Mothers completed self-reports of childhood trauma, prenatal stress, postnatal stress, and physician diagnosis of offspring atopy; provided blood samples to assess physiological responses to chronic stress exposure; and participated in a behavioral task with their infant. RESULTS: Maternal self-reports of childhood trauma, prenatal stress, and postnatal stress were not associated with offspring diagnosis of atopy by 2-3 years of age. Mothers who produced a smaller inflammatory response during pregnancy were more likely to have an offspring with atopy by 2-3 years of age. Warm and responsive parenting demonstrated a protective effect; the positive association between maternal stress and offspring atopy was less apparent in cases of mother-child interactions characterized by high levels warm and responsive parenting. CONCLUSION: Failure to replicate previous findings suggests that the maternal stress-offspring atopy relationship is complex. Future studies must examine the unique stressors in Black Americans, as well as caregiving as a potential protective factor.