PSD was associated with epigenetic signatures at birth, with a subset of associations persisting across early childhood and converging on cellular stress response biology, suggesting differential biological embedding of structural versus psychological dimensions of adversity.
The Barker-consistent hypothesis-free discovery approach identified novel and known candidate genes that, with future validation, may serve as therapeutic targets, identify high-risk individuals, and support clinical trial recruitment.
John Yen Tang, N. Ng, A. S. Kwok et al.· Journal of Global Health· 0 citations
It is found that genomic associations with cord blood DNAm are stronger and more widespread than prenatal exposures, although typically, the prenatal exposome explains additional variation in DNAm beyond genetic influences.
Rosa H. Mulder, Elena Isaevska, C. Cappadona et al.· bioRxiv· 0 citations
A role of DNAm at birth in mediating the association of maternal smoking, birth weight and ADHD-related genetic variants with ADHD symptoms is demonstrated, however, lack of individual site-specific findings and the observational design limit causal biological interpretations.
A. Neumann, M. Suderman, J. Felix et al.· medRxiv· 0 citations
Background. Cord blood DNA methylation profile scores (MPSs) based on genetic and pre-/perinatal risk factors for neurodevelopmental conditions (NDCs) may capture downstream biological effects and help understand how combined exposure signals contribute to NDC risk. Methods. Using data from two longitudinal birth cohorts, Generation R (N-train = 1856, N-test = 476) and ALSPAC (N-validation= 832), we developed cord blood MPSs based on genetic and pre-/perinatal NDC risk factors. We assessed individual and combined predictive performance of risk factors and MPSs for eight childhood psychiatric outcomes (four broad, four specific), measured between ages 5 and 14 years. We also evaluated if the MPSs could be combined into a composite "transmission load" MPS. Results. We validated four novel MPSs: maternal age, birthweight, and genetic liability for ADHD and schizophrenia (r range = 0.08 to 0.29) and included two previously validated MPSs: maternal smoking and gestational age (r range = 0.42 to 0.63). Jointly modeling the six MPSs with their corresponding risk factors explained on average 3.3% of variance in outcomes, higher than that explained by risk factors (1.8%) or MPSs alone (1.6%), indicating complementary sources of risk. The "transmission load" MPS did not replicate due to heterogeneous contributions of the predictors across cohorts. Conclusions. The four novel MPSs based on genetic and pre-/perinatal risk factors can serve as valuable tools for future research. Integrating genetic and prenatal risk factors with DNA methylation at birth can provide insights into their individual and joint contributions to early psychiatric risk and may improve prediction.
Elena Isaevska, Rosa H. Mulder, I. Schuurmans et al.· medRxiv· 0 citations
Birth into neighborhoods characterized by high residential instability and single- person households, and highway proximity was associated with increasing Wu EAA trajectories across childhood, suggesting that early-life neighborhood conditions, encompassing both social and physical environmental factors, may represent targets for interventions aimed at reducing long-term disease risk.
Q.-E. Yuan, A. Bozack, V. Paquin et al.· medRxiv· 0 citations
Parental stress can have lasting consequences on children’s stress sensitivity and self-regulation capacities. However, it remains unclear the extent to which these effects reflect birth parent influences (genetic and/or prenatal), environmental rearing experiences, and/or interactions between them. Parent–offspring adoption designs offer a powerful framework for disentangling these mechanisms by separating birth parent influences from post-natal environmental pathways when the adoptions occur around the time of birth. Although stress experiences of birth parents and adoptive parents have each been associated with child developmental outcomes, the relationship between them remains unexplored. The present study leverages a parent-offspring adoption approach to examine the associations of birth mother life stress with adolescents’ effortful control (EC) via child diurnal cortisol slopes (a marker of hypothalamic–pituitary–adrenal [HPA] axis functioning) and whether adoptive mothers’ or fathers’ experience of stressful life events moderate this relationship. Participants were drawn from families participating in the longitudinal Early Growth and Development Study. The analytic sample included 561 adopted children, and their birth and adoptive parents. Structural equation modeling revealed that birth mother life stress was linked to poorer adoptee EC in adolescence; neither adoptive mothers’ nor fathers’ experiences of stressful life events predicted adoptee EC. Among adoptive parents, only fathers’ experiences of stressful life events predicted child diurnal cortisol slopes, such that greater adoptive fathers’ stress was linked to flatter adoptee wake-to-bedtime cortisol slopes. However, the hypothesized mediation and moderation effects were not supported. These findings show how the birth parent influences (genetic and/or prenatal) and rearing dimensions of parental stress have differential impacts on the child’s neurobiological functioning and development, where birth mother life stress predicts adolescent self-regulation, and adoptive fathers’ stress predicts child stress sensitivity.
Rebecca E. F. Gordon, Elizabeth J S Bates, J. Ganiban et al.· PLoS ONE· 0 citations
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