Springer Nature
Browse
12884_2015_627_MOESM1_ESM.docx (145.53 kB)

Additional file 1: of Maternal psychiatric disease and epigenetic evidence suggest a common biology for poor fetal growth

Download (145.53 kB)
journal contribution
posted on 2015-08-25, 05:00 authored by Timothy Ciesielski, Carmen Marsit, Scott Williams
Supplemental Materials. a) Table S1. Crude associations between clinical variables and poor fetal growth (SGA/IUGR). b) Table S2. Characteristics of the mother-infant pairs by maternal psychiatric status. c) An explanation of the identification of candidate loci for the epigenetic analyses including: Table S3. Genes with known links to psychiatric disease and poor fetal growth. Table S4. 27 candidate loci with measured placental DNA methylation levels. d) Table S5. Loci with methylation patterns that were significantly associated with poor fetal growth. e) Table S6. Mean methylation levels at 6 candidate loci within strata defined by psychiatric and medication status. f) Table S7. Mean methylation levels at the leptin receptor locus by timing of psychiatric diagnosis among those not on antidepressant medication. g) Table S8. Characteristics of the mother-infant pairs by psychiatric status categories used in the methylation analysis. h) Table S9. Methylation at the leptin receptor locus by prenatal tobacco use among those not on antidepressant medication. i) Table S10. Methylation at the leptin receptor locus by maternal psychiatric status excluding those with prenatal tobacco or antidepressant use. j) Table S11. Odds Ratios for poor fetal growth associated with methylation at LEPR/cg21655790 adjusted for prenatal tobacco use. k) Table S12. Characteristics of the mother-infant pairs included in the methylation data subset compared to those excluded. (DOCX 145 kb)

History