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Available from: Gerald Gartlehner, Jan 09, 2015
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    • "Postpartum depression (PPD) affects almost 13% of women in developed high income communities [1] and may be even more common in developing countries [2] [3]. According to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), PPD is a major depression when symptoms have onset within 5 weeks of childbirth [4]. "
    Dataset: 291029

    • "First, our study population of pregnant women is relatively small and does not entirely represent a random sample, since we noted a high socio-economic status and most women were highly educated. However, our study population shows medium levels of pregnancy-related anxiety and a normal prevalence of depressive symptoms measured by EDS score (Gaynes et al., 2005). The lack of individuals with extreme measures of stress may explain the rather small regression coefficients of some of our findings and more pronounced effects might be detected in a population with more extreme depression or anxiety measures. "
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    ABSTRACT: Epigenetic regulation of imprinted genes during embryonic development is influenced by the prenatal environment. Our aim was to examine the effect of maternal emotional stress and cortisol levels during pregnancy on methylation of imprinted genes IGF2 and GNASXL using umbilical cord blood DNA. Maternal depressed mood (Edinburgh Depression Scale; EDS), pregnancy-related anxiety (PRAQ) and cortisol day profiles were assessed throughout pregnancy. At birth, a cord blood sample (n = 80) was taken to study DNA methylation of IGF2 DMR0, IGF2AS and GNASXL using Sequenom EpiTYPER. Linear mixed models were used to examine the relationship between DNA methylation and maternal stress, while correcting for confounders. We also studied the association of DNA methylation with the child ponderal index at birth. We found a CpG-specific association of PRAQ subscales with IGF2 DMR0 (CpG5, p<0.0001) and GNASXL (CpG11, p=0.0003), while IGF2AS was associated with maternal EDS scores (CpG33, p=0.0003) and cortisol levels (CpG33, p=0.0006; CpG37-38, p=0.0005). However, there was no association of methylation with ponderal index at birth. In conclusion, maternal stress during pregnancy, as defined by cortisol measurements, EDS and PRAQ scores, is associated with DNA methylation of imprinted genes IGF2 and GNASXL. Our results provide further evidence that prenatal adversity can influence imprinted gene methylation, although future studies are needed to unravel the exact mechanisms. This article is protected by copyright. All rights reserved.
    Genes Brain and Behavior 09/2015; 61. DOI:10.1111/gbb.12249 · 3.66 Impact Factor
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    • "Women often experience elevated symptoms of postpartum depression ( PPD ) with a prevalence up to 19% ( Gaynes et al . , 2005 ; O ' Hara and McCabe , 2013 ; Wisner et al . , 2013 ) . This can place infants at increased risk for poor behavioral , cognitive , and social development ( Beck , 1998 ; Tronick and Reck , 2009 ). Various psycho - social stress related risk factors for PPD have been defined ( e. g. , low social support and adversity ) and heritability "
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    ABSTRACT: Postpartum depression (PPD) affects up to 19% of women, negatively impacting maternal and infant health. Reductions in plasma oxytocin levels have been associated with PPD and heritability studies have established a genetic contribution. Epigenetic regulation of the oxytocin receptor gene (OXTR) has been demonstrated and we hypothesized that individual epigenetic variability at OXTR may impact the development of PPD and that such variability may be central to predicting risk. This case-control study is nested within the Avon Longitudinal Study of Parents and Children and included 269 cases with PPD and 276 controls matched on age group, parity, and presence or absence of depressive symptoms in pregnancy as assessed by the Edinburgh Postnatal Depression Scale. OXTR DNA methylation (CpG site -934) and genotype (rs53576 and rs2254298) were assayed from DNA extracted from blood collected during pregnancy. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association of elevated symptoms of PPD with genotype, methylation, and their interaction adjusted for psychosocial factors (n = 500). There was evidence of an interaction between rs53576 and methylation in the OXTR gene amongst women who did not have depression prenatally but developed PPD (p interaction = 0.026, adjusted for covariates, n = 257). Those women with GG genotype showed 2.63 greater odds of PPD for every 10% increase in methylation level (95% CI: 1.37, 5.03), whereas methylation was unrelated to PPD amongst "A" carriers (OR = 1.00, 95% CI: 0.58, 1.73). There was no such interaction among women with PPD and prenatal depression. These data indicate that epigenetic variation that decreases expression of OXTR in a susceptible genotype may play a contributory role in the etiology of PPD.
    Frontiers in Genetics 08/2015; 6:243. DOI:10.3389/fgene.2015.00243
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