Treatment of postnatal depression.
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ABSTRACT:
SUBMITTER: Hendrick V
PROVIDER: S-EPMC261646 | biostudies-literature | 2003 Nov
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC8094614 | biostudies-literature
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| S-EPMC6494522 | biostudies-literature
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| S-EPMC558516 | biostudies-literature
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| S-EPMC1590037 | biostudies-literature
Project description:To identify early predictive biomarkers for postpartum depression using peripheral blood gene expression profiles RNA was isolated from peripheral blood collected in Tempus RNA tubes (Applied Biosystems, Darmstadt, Germany) at all three investigated time points for each woman in the discovery sample. RNA was isolated using the Versagene kit (Gentra Systems, Minneapolis, U.S.A.), quantified using the Nanophotometer and quality checks were performed on the Agilent Bioanalyzer.
2013-03-29 | E-GEOD-45603 | biostudies-arrayexpress
Project description:To identify early predictive biomarkers for postpartum depression using peripheral blood gene expression profiles
2013-03-29 | GSE45603 | GEO
Project description:PurposeLack of social support is considered a potential risk factor for postnatal depression but limited longitudinal evidence is available. Pregnancy, when women have increased contact with healthcare services, may be an opportune time to intervene and help strengthen women's social networks to prevent feelings of depression postnatally, particularly for those at greatest risk. Our study examined the longitudinal relationship between social support in pregnancy and postnatal depression, and whether this is moderated by age or relationship status.MethodsWe analysed data collected from 525 women from a diverse inner-city maternity population in England who were interviewed in pregnancy and again three months postnatally. Women provided sociodemographic information and completed self-report measures of depression (Edinburgh Postnatal Depression Scale) and social support (Social Provisions Scale).ResultsLess social support in pregnancy was associated with postnatal depression, after adjusting for sociodemographic confounders and antenatal depression (Coef. = - 0.05; 95% CI - 0.10 to - 0.01; p = 0.02). There was weak evidence of a moderating effect of relationship status. Subgroup analysis showed a stronger relationship between social support in pregnancy and postnatal depression for women who were not living with a partner (Coef. = - 0.11; 95% CI - 0.21 to - 0.01; p = 0.03) than for those who were (Coef. = - 0.03; 95% CI - 0.09 to 0.02; p = 0.28). Sensitivity analysis using multiple imputations to account for missing data confirmed the main results.ConclusionsInterventions that target social support in pregnancy have the potential to reduce depression postnatally. Future research should explore in greater detail which women would benefit most from which type of social support.
| S-EPMC9246777 | biostudies-literature
Project description:Background and objectivesPostnatal depression (PND) presents a puzzling phenomenon to evolutionary anthropologists as it is highly prevalent and yet detrimental to child development and maternal health. Adaptive explanations have been proposed, but have not been tested with data that directly link PND to female fertility.MethodologyA survey was designed to gather complete reproductive histories and retrospective measures of PND to measure the effects of PND on fitness. Respondents were born between 1930 and 1967, with the majority based in the UK during their childrearing years. The hypothesis that PND is detrimental to fitness is assessed using Mann-Whitney U tests on completed fertility. Binary logistic regression modelling is used to test the hypothesis that PND reduces the likelihood of parity progression.ResultsWomen experiencing PND at their first or second birth have lower completed fertility, with PND at the first birth leading to lowered fertility. Logistic regression analyses show that this is the result of reductions in the likelihood of parity progression to a third birth when PND is experienced at the first birth or when repeat bouts occur.Conclusions and implicationsOur results call into question adaptationist arguments, contribute to the growing understanding of the importance of emotional wellbeing to fertility decision making, and given the economic consequences of markedly below replacement fertility, highlight a potential new source of financial incentive to invest in screening and preventative measures to ensure good maternal mental health.
| S-EPMC4790780 | biostudies-literature
Project description:Fluoxetine treatment in adulthood evokes antidepressant and anxiolytic responses. Paradoxically, postnatal fluoxetine (PNFlx) induces persistent depression- and anxiety-like behaviors. The mechanistic underpinnings of this paradox remain poorly understood. Here, we examined specific molecular changes in the rat hippocampus that accompany perturbed emotionality observed across life following PNFlx. PNFlx-induced hippocampal gene regulation observed in microarray and quantitative PCR studies indicate functional enrichment of genes involved in response to organic substances, protein kinase pathways, DNA binding, and transcriptional repression. We noted specific transcripts (Hdac4, mammalian target of rapamycin (mTOR), Gnai1, protein kinase C gamma (Prkcc), and hyperpolarization-activated cyclic nucleotide-gated channel 1 (Hcn1)) that were consistently dysregulated across life, and selectively influenced by postnatal, but not adult, fluoxetine. Increased histone deacetylase-4 (HDAC4) recruitment, accompanied by decreased activating histone acetylation marks at the mTOR and Gnai1 promoters, indicate a role for HDAC4 in PNFlx-mediated gene dysregulation. Strikingly, coadministration of the HDAC inhibitor sodium butyrate with PNFlx prevented the dysregulation of Hdac4 and mTOR, and the emergence of depression- and anxiety-like behavior. Importantly, we also find that retreatment of PNFlx animals with fluoxetine in adulthood reversed the increased Hdac4 expression, prevented HDAC4 recruitment to the mTOR and Gnai1 promoters, and attenuated the decline in mTOR and Gnai1 expression, coincident with normalization of PNFlx-evoked depression- and anxiety-like behavior. Further, we show that viral-mediated hippocampal overexpression of Hdac4 was sufficient to induce depression-, but not anxiety-, like behavior in adulthood. Our results highlight the unique nature of molecular signatures evoked by PNFlx, and implicate HDAC4 in the dysregulated gene expression and emergence of perturbed emotionality following fluoxetine exposure in early life.
| S-EPMC4104341 | biostudies-literature
Project description:BackgroundPrevious studies have reported postpartum depression to be associated with both positive and negative effects on early infant growth. This study examined the hypothesis that maternal postnatal depression may be a risk factor for later child growth faltering or overweight.MethodsA total of 929 women and their children participating in a European multicenter study were included at a median age of 14 days. Mothers completed the Edinburgh postnatal depression scale (EPDS) at 2, 3 and 6 months after delivery. EPDS scores of 13 and above at any time were defined as maternal depression. Weight, length, triceps and subscapular skinfold thicknesses were measured, and body mass index (BMI) were calculated when the children were two years old and converted to standard deviation scores based on the WHO Multicentre Growth Reference Study (MGRS).ResultsZ-scores for weight-for-length at inclusion of infants of mothers with high EPDS scores (-0.55, SD 0.74) were lower than of those with normal scores (-0.36, SD 0.74; p = 0.013). BMI at age 24 months did not differ in the high (16.3 kg/m2, SD 1.3) and in the normal EPDS groups (16.2 kg/m2, SD 1.3; p = 0.48). All other anthropometric indices also did not differ between groups, with no change by multivariate adjustment.ConclusionsWe conclude that a high maternal postnatal depression score does not have any major effects on offspring growth in high income countries.
| S-EPMC2850333 | biostudies-literature