Prenatal stress and epigenetics

Cao-Lei, Lei; Rooij, Susanne R. de; King, Suzanne; Matthews, Stephen G.; Metz, Gerlinde A. S.; Roseboom, Tessa J.; Szyf, Moshe

doi:10.1016/j.neubiorev.2017.05.016

Cited by 163 publications

(112 citation statements)

References 158 publications

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“…More studies are required to understand the underlying fundamental molecular mechanisms related to the role of the interactions between genome, epigenome, maternal environment and postnatal environment. PS through stress hormones or through other pathophysiological and/or genetic mechanisms may program lifespan offspring's stress biology, probably via epigenetic mechanisms [66]. It has been demonstrated that PS can lead to an increase in DNA methylation at specific CpG sites within the 11β-HSD2 gene promoter in the placenta [67].…”

Section: Discussionmentioning

confidence: 99%

Systematic review and meta-analysis on the relationship between prenatal stress and metabolic syndrome intermediate phenotypes

et al. 2019

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Background Metabolic Syndrome (MetS) can be considered as a consequence of a complex interplay between genetic and environmental factors and can be influenced by changes in the environment early in life. Prenatal stress (PS) exposure likely represents an important adverse intrauterine environment that may impact the biology of the developing organism. The aim of this study was to quantitatively synthesize the available data on the effects of PS on offspring's obesity, estimated indirectly by body mass index (BMI) and body fat; blood pressure, plasma glucose and blood lipid concentrations (triglycerides and high-density lipoprotein cholesterol).

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Section: Discussionmentioning

confidence: 99%

Systematic review and meta-analysis on the relationship between prenatal stress and metabolic syndrome intermediate phenotypes

et al. 2019

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“…Prenatal maternal stress (PNMS) increases fetal exposure to stress biomarkers (e.g., cortisol and pro-inflammatory cytokines) and may alter the development of critical biological systems (e.g., the endocrine, immune, and nervous systems) [8, 9, 10]. This confers lasting susceptibility to health complications in the child [2, 4, 5, 6] and potentially transgenerational risks through epigenetic programming [8, 9, 11]. There is also accumulating evidence that the child’s biological sex may modify the effect of PNMS on child health [12, 13, 14, 15].…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in Vulnerability to Prenatal Stress: a Review of the Recent Literature

Sutherland

Brunwasser

2018

Curr Psychiatry Rep

132

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Most articles (k = 35) found evidence of either sex-specific associations (significant in one sex but not the other) or significant PNMSstress interactions for at least one child health outcome. Evidence for sex-dependent effects was strongest in the group of studies evaluating child neural/nervous system development and temperament as outcomes. There is sufficient evidence of sex-dependent associations to recommend that researchers always consider the potential role of child sex in PNMS programming studies and report descriptive statistics for study outcomes stratified by child biological sex.

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“…Epigenetic processes represent a major regulatory mechanism by which the environment modulates gene transcription during development and may explain the decrease of cellular plasticity by the establishment of cell-specific epigenetic profiles during development 26 . Moreover, epigenetic processes are responsible for transgenerational inheritance in several complex traits [27][28][29] . Epigenetics studies focus on three related molecular mechanisms for genome regulation: deoxyribonucleic acid (DNA) modifications, histone modifications and non-coding ribonucleic acids (ncRNAs) [30][31][32][33][34][35][36][37][38][39][40][41] .…”

Section: Developmental Plasticity and Epigenetic Processesmentioning

confidence: 99%

Sleep Apnoea and Early Antecedents of Adult Disease

Gozal¹

2018

BRN

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Obstructive sleep apnoea (OSA) is a highly prevalent disorder across the life spectrum including early childhood and pregnancy. Occurrence of sleep perturbations and intermittent hypoxia that constitute major hallmarks of OSA during these favourable developmental plasticity windows may facilitate emergence of incremental risks for a variety of ageing-related disorders via a multitude of epigenetic mechanisms. In addition, OSA during late adolescence and adulthood is not immune to epigenetic changes, the latter potentially playing a role in the reversibility of OSA-associated morbidities upon implementation of therapy. Furthermore, unique epigenetic signatures may provide powerful biomarkers for precision-based medicine approaches in the framework of OSA. Taken together, the conceptual umbrellas assigning major roles to epigenetics in the context of OSA-associated phenotypic expression and longitudinal disease risk trajectories is not a farfetched idea any longer. Early adoption of these biologically relevant principles and their implementation to the upcoming future clinical trials appears inevitable if progress is to occur. (BRN Rev. 2018;4(3):185-99)

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Prenatal stress and epigenetics

Cited by 163 publications

References 158 publications

Systematic review and meta-analysis on the relationship between prenatal stress and metabolic syndrome intermediate phenotypes

Systematic review and meta-analysis on the relationship between prenatal stress and metabolic syndrome intermediate phenotypes

Sex Differences in Vulnerability to Prenatal Stress: a Review of the Recent Literature

Sleep Apnoea and Early Antecedents of Adult Disease

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