Placental DNA methylation changes associated with maternal prepregnancy BMI and gestational weight gain.
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ABSTRACT:
SUBMITTER: Shrestha D
PROVIDER: S-EPMC7261634 | biostudies-literature | 2020 Jun
REPOSITORIES: biostudies-literature
Publications
Placental DNA methylation changes associated with maternal prepregnancy BMI and gestational weight gain.
Shrestha Deepika D Ouidir Marion M Workalemahu Tsegaselassie T Zeng Xuehuo X Tekola-Ayele Fasil F
International journal of obesity (2005) 20200218 6
<h4>Background</h4>Maternal obesity prior to or during pregnancy influences fetal growth, predisposing the offspring to increased risk for obesity across the life course. Placental epigenetic mechanisms may underlie these associations. We conducted an epigenome-wide association study to identify placental DNA methylation changes associated with maternal prepregnancy body mass index (BMI) and rate of gestational weight gain at first (GWG1), second (GWG2), and third trimester (GWG3).<h4>Method</h4 ...[more]
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| S-EPMC4827014 | biostudies-other
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| S-EPMC3869661 | biostudies-literature
Project description:ObjectivesWe aimed to discover CpG sites with differential DNA methylation in peripheral blood leukocytes associated with body mass index (BMI) in pregnancy and gestational weight gain (GWG) in women of European and South Asian ancestry. Furthermore, we aimed to investigate how the identified sites were associated with methylation quantitative trait loci, gene ontology, and cardiometabolic parameters.MethodsIn the Epigenetics in pregnancy (EPIPREG) sample we quantified maternal DNA methylation in peripheral blood leukocytes in gestational week 28 with Illumina's MethylationEPIC BeadChip. In women with European (n = 303) and South Asian (n = 164) ancestry, we performed an epigenome-wide association study of BMI in gestational week 28 and GWG between gestational weeks 15 and 28 using a meta-analysis approach. Replication was performed in the Norwegian Mother, Father, and Child Cohort Study, the Study of Assisted Reproductive Technologies (MoBa-START) (n = 877, mainly European/Norwegian).ResultsWe identified one CpG site significantly associated with GWG (p 5.8 × 10-8) and five CpG sites associated with BMI at gestational week 28 (p from 4.0 × 10-8 to 2.1 × 10-10). Of these, we were able to replicate three in MoBa-START; cg02786370, cg19758958 and cg10472537. Two sites are located in genes previously associated with blood pressure and BMI. DNA methylation at the three replicated CpG sites were associated with levels of blood pressure, lipids and glucose in EPIPREG (p from 1.2 × 10-8 to 0.04).ConclusionsWe identified five CpG sites associated with BMI at gestational week 28, and one with GWG. Three of the sites were replicated in an independent cohort. Several genetic variants were associated with DNA methylation at cg02786379 and cg16733643 suggesting a genetic component influencing differential methylation. The identified CpG sites were associated with cardiometabolic traits.ClinicaltrialsGov registration noNot applicable.
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Project description:ObjectiveGestational weight gain (GWG) above recommendations is a risk factor for adverse maternal, perinatal, and long-term outcomes. This study hypothesized that prepregnancy weight gain may portend excess GWG.MethodsAmong 1,126 women (51% of whom were of Black race) in the Coronary Artery Risk Development in Young Adults (CARDIA) study with post-baseline births, the prepregnancy annual rate of BMI change per woman was estimated (slope; 5 years before pregnancy) and was related to the risk of GWG above Institute of Medicine recommendations using mixed-effects models (binary) and GWG z score (continuous), adjusting for confounders, and stratified by prepregnancy overweight/obesity status.ResultsA total of 626 women (56%) had excess GWG. Each standard deviation increase in prepregnancy BMI (0.16 kg/m2 per year) was associated with an 18% increased risk of excess GWG (95% CI: 1.13-1.23), adjusted for covariates. Stratified results showed an association for women without overweight or obesity (adjusted relative risk = 1.71 [95% CI: 1.38-2.13]) but not among those with overweight or obesity (adjusted relative risk = 0.98 [95% CI: 0.91-1.05]). When evaluated as a z score, prepregnancy weight gain was associated with higher GWG among women with and without overweight or obesity (mean = 0.24 [0.10] and 0.28 [0.12] z score, respectively).ConclusionsWeight gain before pregnancy is associated with higher GWG during pregnancy. Assessment of prepregnancy weight changes may identify those at risk for high GWG.
| S-EPMC9996907 | biostudies-literature
Project description:Pre-existing maternal overweight/obesity and pregnancy weight gain are associated with adverse birth outcomes such as low birth weight and prematurity, which may increase the risk of developmental tooth defects and early childhood caries. We sought to investigate the association between prepregnancy BMI, gestational weight gain (GWG) and the risk of early childhood caries. Data from 1,429 mother-offspring participants of the 1991/1992 Avon Longitudinal Study of Parents and Children were analyzed. The exposures were prepregnancy BMI (under/normal weight vs. overweight/obese), and gestational weight gain (GWG) based on the Institute of Medicine's recommended levels. The main outcome measured was offspring caries experience determined by clinical oral examinations at three time points. Log binomial regression estimated risk ratios and 95% confidence intervals. Seventy six percent (76%) of the mothers were under/normal weight prepregnancy, 39% and 26% respectively gained less and more than the recommended weight for their prepregnancy BMI during pregnancy. Being overweight/obese prepregnancy was associated with unadjusted RR (95% CI) of offspring caries of 1.16 (0.90, 1.51) at 31-months, 1.20 (0.96, 1.49) at 43-months and 1.09 (0.91, 1.30) at 61-months. GWG less than recommended was associated with higher unadjusted offspring caries experience of 1.13 (0.86, 1.48), 1.17 (0.92, 1.48) and 1.04 (0.87, 1.25) at 31-months, 43-months and 61-months respectively. There was insufficient evidence to indicate an association between prepregnancy BMI and gestational weight gain on offspring caries experience risk.
| S-EPMC8970488 | biostudies-literature
Project description:ObjectiveMaternal prepregnancy BMI and gestational weight gain (GWG) are examined in relation to autism spectrum disorder (ASD) and other developmental disorders (DD) in offspring in a multisite case-control study.MethodsMaternal prepregnancy BMI, obtained from medical records or self-report, was categorized as underweight, normal weight, overweight, obesity Class 1, or obesity Class 2/3. GWG was standardized for gestational age (GWG z score), and the rate (pounds/week) was categorized per adherence with clinical recommendations. Logistic regression models, adjusting for demographic factors, were used to assess associations with ASD (n = 1,159) and DD (n = 1,617), versus control children (n = 1,633).ResultsMaternal obesity Class 2/3 was associated with ASD (adjusted odds ratio [AOR] = 1.87, 95% CI: 1.40-2.51) and DD (AOR = 1.61, 95% CI: 1.22-2.13). GWG z score was not associated with DD (AOR = 1.14, 95% CI: 0.95-1.36), but the GWG z score highest tertile was associated with higher odds of ASD, particularly among male children (AOR = 1.47, 95% CI: 1.15-1.88).ConclusionsResults indicate that maternal prepregnancy severe obesity increases risk of ASD and DD in children and suggest high gestational-age-adjusted GWG is a risk factor for ASD in male children. Because maternal BMI and GWG are routinely measured and potentially modifiable, these findings could inform early interventions for high-risk mother-child dyads.
| S-EPMC9186321 | biostudies-literature