Who is distressed? A comparison of psychosocial stress in pregnancy across seven ethnicities.

BACKGROUND: Calgary, Alberta has the fourth highest immigrant population in Canada and ethnic minorities comprise 28 % of its total population. Previous studies have found correlations between minority status and poor pregnancy outcomes. One explanation for this phenomenon is that minority status increases the levels of stress experienced during pregnancy. The aim of the present study was to identify specific types of maternal psychosocial stress experienced by women of an ethnic minority (Asian, Arab, Other Asian, African, First Nations and Latin American). METHODS: A secondary analysis of variables that may contribute to maternal psychosocial stress was conducted using data from the All Our Babies prospective pregnancy cohort (N = 3,552) where questionnaires were completed at < 24 weeks of gestation and between 34 and 36 weeks of gestation. Questionnaires included standardized measures of perceived stress, anxiety, depression, physical and emotional health, and social support. Socio-demographic data included immigration status, language proficiency in English, ethnicity, age, and socio-economic status. RESULTS: Findings from this study indicate that women who identify with an ethnic minority were more likely to report symptoms of depression, anxiety, inadequate social support, and problems with emotional and physical health during pregnancy than women who identified with the White reference group. CONCLUSIONS: This study has identified that women of an ethic minority experience greater psychosocial stress in pregnancy compared to the White reference group.

Ancestral exposure to stress epigenetically programs preterm birth risk and adverse maternal and newborn outcomes.

BACKGROUND: Chronic stress is considered to be one of many causes of human preterm birth (PTB), but no direct evidence has yet been provided. Here we show in rats that stress across generations has downstream effects on endocrine, metabolic and behavioural manifestations of PTB possibly via microRNA (miRNA) regulation. METHODS: Pregnant dams of the parental generation were exposed to stress from gestational days 12 to 18. Their pregnant daughters (F1) and grand-daughters (F2) either were stressed or remained as non-stressed controls. Gestational length, maternal gestational weight gain, blood glucose and plasma corticosterone levels, litter size and offspring weight gain from postnatal days 1 to 30 were recorded in each generation, including F3. Maternal behaviours were analysed for the first hour after completed parturition, and offspring sensorimotor development was recorded on postnatal day (P) 7. F0 through F2 maternal brain frontal cortex, uterus and placenta miRNA and gene expression patterns were used to identify stress-induced epigenetic regulatory pathways of maternal behaviour and pregnancy maintenance. RESULTS: Progressively up to the F2 generation, stress gradually reduced gestational length, maternal weight gain and behavioural activity, and increased blood glucose levels. Reduced offspring growth and delayed behavioural development in the stress cohort was recognizable as early as P7, with the greatest effect in the F3 offspring of transgenerationally stressed mothers. Furthermore, stress altered miRNA expression patterns in the brain and uterus of F2 mothers, including the miR-200 family, which regulates pathways related to brain plasticity and parturition, respectively. Main miR-200 family target genes in the uterus, Stat5b, Zeb1 and Zeb2, were downregulated by multigenerational stress in the F1 generation. Zeb2 was also reduced in the stressed F2 generation, suggesting a causal mechanism for disturbed pregnancy maintenance. Additionally, stress increased placental miR-181a, a marker of human PTB. CONCLUSIONS: The findings indicate that a family history of stress may program central and peripheral pathways regulating gestational length and maternal and newborn health outcomes in the maternal lineage. This new paradigm may model the origin of many human PTB causes.