An Audit of Pre-Pregnancy Maternal Obesity and Diabetes Screening in Rural Regional Tasmania and Its Impact on Pregnancy and Neonatal Outcomes.
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ABSTRACT:
SUBMITTER: Luccisano SP
PROVIDER: S-EPMC8619569 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Neonatal adiposity has many determinants and may be a risk factor for future obesity. Epigenetic regulation of metabolically important genes is a potential contributor.The objective of the study is to determine whether methylation changes in the LEP gene in cord blood DNA are impacted by the maternal environment or affect neonatal adiposity measures.A cross-sectional study of 114 full-term neonates born to healthy mothers with normal glucose tolerance was performed. Cord blood was assayed for leptin and genome-wide DNA methylation profiles via the Illumina 450K platform. Neonatal body composition was measured by air displacement plethysmography. Multivariate linear regression models and semi-partial correlation coefficients were used to analyze associations. False discovery rate was estimated to account for multiple comparisons.Maternal pre-pregnancy BMI was associated with decreased methylation at five CpG sites near the LEP transcription start site in an adjusted model (false discovery rate <0.022 for each site). The association between maternal BMI and cord blood leptin approached significance (r?=?0.18, p?=?0.054). Cord blood leptin was positively correlated with neonatal adiposity measures including birth weight (r?=?0.45, p?<?0.001), fat mass (r?=?0.47, p?<?0.001) and percent body fat (r?=?0.44, p?<?0.001).Maternal pre-pregnancy BMI is strongly associated with decreased cord blood LEP gene methylation and may mediate the well-known association between maternal pre-pregnancy BMI and neonatal adiposity.
| S-EPMC5462869 | biostudies-literature
Project description:IntroductionBMI is a tool to measure maternal nutritional status. Maternal malnutrition is frequently reported health problem especially during child bearing age and effects neonatal birth weight.AimTo determine relationship between prepregnancy maternal BMI and neonatal birth weight.Methods and materialProspective, cross sectional study conducted in Fatima Memorial Hospital, Lahore, Pakistan over a period of 1 year including 2766 mother-neonate pairs. All full term, live born neonates of both gender in early neonatal period (<72 hours) with documented maternal pre-pregnancy and/or first trimester BMI were enrolled. Data analysis using SPSS version 20, was performed.ResultsData analysis of 2766 mother-neonates pairs showed that there were 32.9% overweight and 16.5% obese mothers. More than two third of all overweight and obese mothers were of age group between 26-35 years. Diabetes mellitus, hypertension, medical illness, uterine malformations and caesarean mode of delivery were more prevalent in obese mothers as 22.8%, 10.1%, 13.2%, 2.6% and 75.4% respectively. Mean birth weight, length and OFC increased with increasing maternal BMI. Comparing for normal weight mothers, underweight mothers were at increased risk of low birth weight (p< 0.01) and low risk of macrosomic neonates (p<0.01). However overweight and obese mothers were comparable to normal weight mothers for delivering macrosomic neonates (p 0.89 and p 0.66 respectively).ConclusionsOur study highlights that direct relationship exists between maternal BMI and neonatal birth weight.
| S-EPMC7592734 | biostudies-literature
Project description:Maternal obesity is becoming a major health consideration for successful pregnancy outcomes. There is growing proof that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are so far poorly understood. We set out to analyse term placenta whole transcriptome in obese (n=5) and normoweight women (n=5), using Affymetrix microarray platform compromising of 50,000 probe sets. Our analysis shows that the placental transcriptome differs between normoweight and obese women. Different processes and pathways among placenta from obese women were dysregulated, including inflammation and immune responses, lipid metabolism, cell death and survival and cancer pathways, vasculogenesis and angiogenesis, and glucocorticoid receptor signaling pathway. Together, this global gene expression profiling approach demonstrates and confirms that maternal obesity creates a unique in utero environment that impairs placental transcriptome.
2017-01-07 | E-MTAB-4541 | biostudies-arrayexpress
Project description:A number of studies have linked obesity with asthma in adults and children. Few longitudinal studies have evaluated the effect of maternal pre-pregnancy obesity on either asthma or early childhood respiratory morbidity, and these have not been in urban, nonwhite populations. We sought to determine whether pre-pregnancy obesity was associated with recurrent wheezing in an urban, nonwhite population. This study includes 1,191 children from the Boston Birth Cohort (1998-present) followed prospectively to a mean age of 3.0?±?2.4 years with study visits aligned with the pediatric primary care schedule. Multivariate logistic regression was used to evaluate the associations of maternal pre-pregnancy obesity (body mass index ?30) with recurrent wheezing (?4 lifetime episodes). Secondary outcomes included log-transformed cord-blood immunoglobulin E (Phadia), and physician diagnoses of eczema and food allergy. Pre-pregnancy obesity was present in 20.7% of mothers. Of the 1,191 children, 60 (5%) developed recurrent wheezing. Children of obese mothers had an increased risk of recurrent wheezing (adjusted odds ratio, 95% confidence interval: 3.51, 1.68-7.32). These associations persisted even after adjustment for fetal growth status. In contrast, maternal obesity was not associated with eczema or food allergy, and was inversely associated with log cord-blood immunoglobulin E (?, 95% confidence interval: -0.34, -0.66 to -0.02). In this predominantly urban, multiracial/ethnic birth cohort, maternal pre-pregnancy obesity was associated with an increased risk of recurrent wheezing. This association was not explained by fetal growth or increased atopy. Maternal pre-pregnancy obesity is a prevalent risk factor for respiratory morbidity in this urban, nonwhite population.
| S-EPMC3281288 | biostudies-literature
Project description:Maternal obesity has a major impact on pregnancy outcomes. There is growing evidence that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are poorly understood. We analysed ten term placenta's whole transcriptomes in obese (n = 5) and normal weight women (n = 5), using the Affymetrix microarray platform. Analyses of expression data were carried out using non-parametric methods. Hierarchical clustering and principal component analysis showed a clear distinction in placental transcriptome between obese and normal weight women. We identified 72 differentially regulated genes, with most being down-regulated in obesity (n = 61). Functional analyses of the targets using DAVID and IPA confirm the dysregulation of previously identified processes and pathways in the placenta from obese women, including inflammation and immune responses, lipid metabolism, cancer pathways, and angiogenesis. In addition, we detected new molecular aspects of obesity-derived effects on the placenta, involving the glucocorticoid receptor signalling pathway and dysregulation of several genes including CCL2, FSTL3, IGFBP1, MMP12, PRG2, PRL, QSOX1, SERPINE2 and TAC3. Our global gene expression profiling approach demonstrates that maternal obesity creates a unique in utero environment that impairs the placental transcriptome.
| S-EPMC5268451 | biostudies-literature
Project description:Maternal obesity is associated with adverse offspring outcomes. Inflammation and deficiency of anti-inflammatory nutrients like omega(n)-3 polyunsaturated fatty acids (PUFA) may contribute to these associations. Fetal supply of n-3 PUFA is dependent on maternal levels and studies have suggested that improved offspring outcomes are associated with higher maternal intake. However, little is known about how maternal obesity affects the response to n-3 supplementation during pregnancy. We sought to determine (1) the associations of obesity with PUFA concentrations and (2) if the systemic response to n-3 supplementation differs by body mass index (BMI). This was a secondary analysis of 556 participants (46% lean, 28% obese) in the Maternal-Fetal Medicine Units Network trial of n-3 (Docosahexaenoic acid (DHA) + Eicosapentaenoic acid (EPA)) supplementation, in which participants had 2g/day of n-3 (n = 278) or placebo (n = 278) from 19 to 22 weeks until delivery. At baseline, obese women had higher plasma n-6 arachidonic acid concentrations (β: 0.96% total fatty acids; 95% Confidence Interval (CI): 0.13, 1.79) and n-6/n-3 ratio (β: 0.26 unit; 95% CI: 0.05, 0.48) compared to lean women. In the adjusted analysis, women in all BMI groups had higher n-3 concentrations following supplementation, although obese women had attenuated changes (β = -2.04%, CI: -3.19, -0.90, interaction p = 0.000) compared to lean women, resulting in a 50% difference in the effect size. Similarly, obese women also had an attenuated reduction (β = 0.94 units, CI: 0.40, 1.47, interaction p = 0.046) in the n-6/n-3 ratio (marker of inflammatory status), which was 65% lower compared to lean women. Obesity is associated with higher inflammation and with an attenuated response to n-3 supplementation in pregnancy.
| S-EPMC6315963 | biostudies-literature
Project description:This review examined evidence of the association between maternal pre-pregnancy overweight/obesity status and child neurodevelopmental outcomes. PubMed and PsycINFO databases were systematically searched for empirical studies published before April 2017 using keywords related to prenatal obesity and children's neurodevelopment. Of 1483 identified papers, 41 were included in the systematic review, and 32 articles representing 36 cohorts were included in the meta-analysis. Findings indicated that compared with children of normal weight mothers, children whose mothers were overweight or obese prior to pregnancy were at increased risk for compromised neurodevelopmental outcomes (overweight: OR = 1.17, 95% CI [1.11, 1.24], I2 = 65.51; obese: OR = 1.51; 95% CI [1.35, 1.69], I2 = 79.63). Pre-pregnancy obesity increased the risk of attention deficit-hyperactivity disorder (OR = 1.62; 95% CI [1.23, 2.14], I2 = 70.15), autism spectrum disorder (OR = 1.36; 95% CI [1.08, 1.70], I2 = 60.52), developmental delay (OR = 1.58; 95% CI [1.39, 1.79], I2 = 75.77) and emotional/behavioural problems (OR = 1.42; 95% CI [1.26, 1.59], I2 = 87.74). Given the current obesity prevalence among young adults and women of childbearing age, this association between maternal obesity during pregnancy and atypical child neurodevelopment represents a potentially high public health burden.
| S-EPMC6059608 | biostudies-literature
Project description:BackgroundOverweight or obesity among pregnant women may compromise maternal and neonatal iron status by upregulating hepcidin.ObjectivesThis study determined the association of 1) maternal and neonatal iron status with maternal and neonatal hepcidin concentrations, and 2) maternal prepregnancy weight status with maternal and neonatal hepcidin concentrations.MethodsWe examined hematologic data from 405 pregnant women and their infants from the placebo treatment group of a pregnancy iron supplementation trial in rural China. We measured hepcidin, serum ferritin (SF), soluble transferrin receptor (sTfR), and high-sensitivity C-reactive protein in maternal blood samples at mid-pregnancy and in cord blood at delivery. We used regression analysis to examine the association of maternal prepregnancy overweight or obese status with maternal hepcidin concentration in mid-pregnancy and cord hepcidin concentrations. We also used path analysis to examine mediation of the association of maternal prepregnancy overweight or obese status with maternal iron status by maternal hepcidin, as well as with neonatal hepcidin by neonatal iron status.ResultsMaternal iron status was positively correlated with maternal hepcidin at mid-pregnancy (SF: r = 0.63, P < 0.001; sTfR: r = -0.37, P < 0.001). Neonatal iron status was also positively correlated with cord hepcidin (SF: r = 0.61, P < 0.001; sTfR: r = -0.39, P < 0.001). In multiple linear regression models, maternal prepregnancy overweight or obese status was not associated with maternal hepcidin at mid-pregnancy but was associated with lower cord hepcidin (coefficient = -0.21, P = 0.004). Using path analysis, we observed a significant indirect effect of maternal prepregnancy overweight or obese status on cord hepcidin, mediated by neonatal iron status.ConclusionsIn both pregnant women and neonates, hepcidin was responsive to iron status. Maternal prepregnancy overweight status, with or without including obese women, was associated with lower cord blood hepcidin, likely driven by lower iron status among the neonates of these mothers.
| S-EPMC8349130 | biostudies-literature
Project description:It is well known that periodontitis, diagnosed mainly by periodontal probing, is associated with adverse pregnancy outcomes. However, periodontal probing is time-consuming, highly discomforting, inaccurate, and invasive. We aimed to assess whether periodontitis severity based on radiological staging in accordance with the 2017 new consensus classification was related to adverse pregnancy and neonatal outcomes. The medical records of 165 mothers who underwent panoramic radiography within 5 years before and after the time of delivery and of their singleton neonates were retrospectively reviewed. Twenty-two mothers (13.3%) had severe periodontitis (SP), and 143 (86.7%) had mild or moderate periodontitis (MP). In relation to adverse pregnancy outcomes, uterine leiomyoma (18.2% vs. 4.2%, P = 0.029), chronic hypertension (9.1% vs. 0.7%, P = 0.047), and preeclampsia (13.6% vs. 2.1%, P = 0.032) occurred significantly more frequently in the SP group than in the MP group. The incidences of very preterm birth (13.6% vs. 1.4%, P = 0.017), extremely preterm birth (9.1% vs. 0.7%, P = 0.047), and small for gestational age (22.7% vs. 5.6%, P = 0.017) were also significantly higher in the SP group than in the MP group. Radiological screening of maternal periodontitis could be useful for predicting adverse pregnancy and neonatal outcomes as well as diagnosing SP in pregnant women.
| S-EPMC7718227 | biostudies-literature
Project description:BackgroundCumulative evidence indicates an association between maternal overweight and gestational diabetes with delayed breastfeeding initiation; however, the presence of both conditions simultaneously has been little explored. This study aims to investigate the interaction between maternal overweight/obesity and gestational diabetes on breastfeeding initiation.MethodsThis study comprises data from the IVAPSA Birth Cohort, a prospective follow-up of mothers and their newborns. Two of the five groups from IVAPSA were evaluated, considering women with and without gestational diabetes. These women were further categorized according to their pre-pregnancy body mass index as normal weight or overweight/obese.Results219 women were evaluated, 53.4% of them had pre-pregnancy overweight/obesity and 32% had gestational diabetes. Most women were able to initiate breastfeeding within 12 hours from delivery (92.7%) and only eight (3.7%) women had not breastfed in the first 24 hours postpartum. Of these, seven were overweight/obese (77.8%) and five had gestational diabetes (66.7%), with four of them having overweight/obesity and gestational diabetes concomitantly. Women with both adverse conditions had an adjusted relative risk of delayed breastfeeding initiation of 1.072 (95% CI 1.006; 1.141), p = 0.032.ConclusionsThe results indicate an additive interaction between maternal pre-pregnancy overweight/obesity and gestational diabetes on delayed breastfeeding initiation.
| S-EPMC6005508 | biostudies-literature