Association between preconception maternal stress and offspring birth weight: findings from an Australian longitudinal data linkage study.
Ontology highlight
ABSTRACT: Objective
Examine the relationship between preconception stress and offspring birth weight.Setting
Population-based cohort study linked with state-based administrative perinatal data.Participants
6100 births from 3622 women from the 1973-1978 cohort of the Australian Longitudinal Study of Women's Health who (1) recorded a singleton birth between January 1997 and December 2011; (2) returned at least one follow-up survey within 3 years of conception; and (3) had complete data on perceived stress prior to conception.Primary outcome measures
Linear generalised estimating equations were used to examine the relationship between preconception stress and a continuous measure of birth weight, exploring differences based on birth order and stress chronicity. The minimal sufficient adjustment set of covariates was determined by a directed acyclic graph.Results
For all births, there was no relationship between moderate/high acute or chronic stress and offspring birth weight in grams. Among first births only, there was a trend towards a relationship between moderate/high chronic stress and offspring birth weight. Offspring sex was associated with birth weight in all models, with female babies born lighter than male babies on average, after adjusting for covariates (p<0.0001).Conclusions
Effects of preconception stress on birth weight was largely driven by time to conception. With the timing of stress critical to its impact on obstetrical outcomes, preconception care should involve not only reproductive life planning but the space to provide interventions at critical periods so that optimal outcomes are achieved.
SUBMITTER: Harris ML
PROVIDER: S-EPMC7942266 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:ObjectivesWe examined the impact of preconception acute and chronic stressors on offspring birth weight and racial/ethnic birth weight disparities.MethodsWe included birth weights for singleton live first (n = 3512) and second (n = 1901) births to White, Mexican-origin Latina, other-origin Latina, and Black women reported at wave IV of the National Longitudinal Study of Adolescent Health (2007-2008; ages 24-32 years). We generated factor scores for preconception acute and chronic stressors from wave I (1994-1995; ages 11-19 years) or wave III (2001-2002; ages 18-26 years) for the same cohort of women.ResultsLinear regression models indicated that chronic stressors, but not acute stressors, were inversely associated with birth weight for both first and second births (b = -192; 95% confidence interval = -270, -113; and b = -180; 95% confidence interval = -315, -45, respectively), and partially explained the disparities in birth weight between the minority racial/ethnic groups and Whites.ConclusionsPreconception chronic stressors contribute to restricted birth weight and to racial/ethnic birth weight disparities.
| S-EPMC4103215 | biostudies-literature
Project description:Rationale:Improved birth weight outcomes have been reported for infants of mothers imprisoned during pregnancy relative to similarly disadvantaged mothers, however, findings are equivocal and evidence is lacking from jurisdictions outside the United States. Objective:To investigate whether maternal imprisonment during pregnancy is a determinant of low birth weight (<2500?g) for Indigenous and non-Indigenous infants in Western Australia. Methods:A longitudinal sample of 41,910 singleton infants born in Western Australia (October 1985-December 2013), was identified with linked administrative data and examined by five mutually exclusive categories of maternal corrections history; (i) imprisonment in pregnancy, (ii) imprisonment before pregnancy, (iii) first imprisonment after birth, (iv) community-based corrections record without imprisonment at any time, and (v) no corrections record at any time. Univariate and multivariate Poisson regression was performed to determine key risk factors for low birth weight. Prevalence of risk factors were calculated by maternal corrections history. Results:After adjusting for other significant pregnancy risks, maternal imprisonment before (Indigenous RR 2.02, 95%CI 1.84-2.22, p<.001; non-Indigenous RR 2.48, 95%CI 1.98-3.12, p<.001) or during (Indigenous RR 1.96, 95%CI 1.68-2.29, p<.001; non-Indigenous RR 2.12, 95%CI 1.48-3.03, p<.001) pregnancy remained strong determinants of low birth weight, and carried greater risk than imprisonment after birth (Indigenous RR 1.58, 95%CI 1.44-1.74, p<.001; non-Indigenous RR 1.75, 95%CI 1.51-2.04, p<.001) or community-based corrections orders (Indigenous RR 1.32, 95%CI 1.21-1.43, p<.001; non-Indigenous RR 1.40, 95%CI 1.05-1.88, p<.001), relative to no corrections record. Pregnancy risk factors more prevalent amongst infants whose mothers were imprisoned before or during pregnancy included substance-use related service contacts, hospitalisation for injury, mental health service contacts, and having a sibling in contact with the child protection system. Conclusion:Western Australian infants with mothers imprisoned before or during pregnancy experience elevated risk of low birth weight and exposure to maternal substance use, injury and mental distress in pregnancy.
| S-EPMC6290037 | biostudies-literature
Project description:Introduction: Maternal nutrition during pregnancy is linked with birth outcomes including fetal growth, birth weight, congenital anomalies and long-term health through intra-uterine programming. However, a woman's nutritional status before pregnancy is a strong determinant in early embryo-placental development, and subsequently outcomes for both mother and child. Therefore, the aim of this study was to investigate the association between dietary macronutrient intake in the preconception period with birth weight.Methods: We studied a group of 1698 women from the Dutch Perined-Lifelines linked birth cohort with reliable detailed information on preconception dietary macronutrient intake (using a semi quantitative food frequency questionnaire) and data available on birth weight of the offspring. Birth weight was converted into gestational age adjusted z-scores, and macronutrient intake was adjusted for total energy intake using the nutrient residual method. Preconception BMI was converted into cohort-based quintiles. Multivariable linear regression was performed, adjusted for other macronutrients and covariates.Results: Mean maternal age was 29.5 years (SD 3.9), preconception BMI: 24.7 kg/m2 (SD 4.2) and median daily energy intake was 1812 kcal (IQR 1544-2140). Mean birth weight was 3578 grams (SD 472). When adjusted for covariates, a significant association (adjusted z score [95% CI], P) between polysaccharides and birth weight was shown (0.08 [0.01-0.15], 0.03). When linear regression analyses were performed within cohort-based quintiles of maternal BMI, positive significant associations between total protein, animal protein, fat, total carbohydrates, mono-disaccharides and polysaccharides with birth weight were shown in the lowest quintile of BMI independent of energy intake, intake of other macronutrients and covariates.Conclusion: Out of all macronutrients studied, polysaccharides showed the strongest association with birth weight, independent of energy intake and other covariates. Our study might suggest that specifically in women with low preconception BMI a larger amount of macronutrient intake was associated with increased birth weight. We recommend that any dietary assessment and advise during preconception should be customized to preconception weight status of the women.
| S-EPMC7710031 | biostudies-literature
Project description:It is well-established that both the child's genetic endowments as well as maternal smoking during pregnancy impact offspring birth weight. In this paper we move beyond the nature versus nurture debate by investigating the interaction between genetic endowments and this critical prenatal environmental exposure - maternal smoking - in determining birth weight. We draw on longitudinal data from the Avon Longitudinal Study of Parents and Children (ALSPAC) study and replicate our results using data from the UK Biobank. Genetic endowments of the children are proxied with a polygenic score that is constructed based on the results of the most recent genome-wide association study of birth weight. We instrument the maternal decision to smoke during pregnancy with a genetic variant (rs1051730) located in the nicotine receptor gene CHRNA3. This genetic variant is associated with the number of cigarettes consumed daily, and we present evidence that this is plausibly the only channel through which the maternal genetic variant affects the child's birth weight. Additionally, we deal with the misreporting of maternal smoking by using measures of cotinine, a biomarker of nicotine, collected from the mother's urine during their pregnancy. We confirm earlier findings that genetic endowments as well as maternal smoking during pregnancy significantly affects the child's birth weight. However, we do not find evidence of meaningful interactions between genetic endowments and an adverse fetal environment, suggesting that the child's genetic predisposition cannot cushion the damaging effects of maternal smoking.
| S-EPMC7654929 | biostudies-literature
Project description:BackgroundObservational studies and randomized controlled trials have found evidence that higher maternal circulating cortisol levels in pregnancy are associated with lower offspring birth weight. However, it is possible that the observational associations are due to residual confounding.MethodsWe performed two-sample Mendelian Randomisation (MR) using a single genetic variant (rs9989237) associated with morning plasma cortisol (GWAS; sample 1; N = 25,314). The association between this maternal genetic variant and offspring birth weight, adjusted for fetal genotype, was obtained from the published EGG Consortium and UK Biobank meta-analysis (GWAS; sample 2; N = up to 406,063) and a Wald ratio was used to estimate the causal effect. We also performed an alternative analysis using all GWAS reported cortisol variants that takes account of linkage disequilibrium. We also tested the genetic variant's effect on pregnancy cortisol and performed PheWas to search for potential pleiotropic effects.ResultsThe estimated effect of maternal circulating cortisol on birth weight was a 50 gram (95% CI, -109 to 10) lower birth weight per 1 SD higher log-transformed maternal circulating cortisol levels, using a single variant. The alternative analysis gave similar results (-33 grams (95% CI, -77 to 11)). The effect of the cortisol variant on pregnancy cortisol was 2-fold weaker than in the original GWAS, and evidence was found of pleiotropy.ConclusionsOur findings provide some evidence that higher maternal morning plasma cortisol causes lower birth weight. Identification of more independent genetic instruments for morning plasma cortisol are necessary to explore the potential bias identified.
| S-EPMC10789047 | biostudies-literature
Project description:In this study, the association between maternal age at menarche (AAM)-related polymorphisms and offspring birth weight (BW) was studied. The work was performed on a sample of 716 pregnant women and their newborns. All pregnant women underwent genotyping of 50 SNPs of AAM candidate genes. Regression methods (linear and Model-Based Multifactor Dimensionality Reduction (MB-MDR)) with permutation procedures (the indicator pperm was calculated) were used to identify the correlation between SNPs and newborn weight (transformed BW values were analyzed) and in silico bioinformatic examination was applied to assess the intended functionality of BW-associated loci. Four AAM-related genetic variants were BW-associated including genes such as POMC (rs7589318) (βadditive = 0.202/pperm = 0.015), KDM3B (rs757647) (βrecessive = 0.323/pperm = 0.005), INHBA (rs1079866) (βadditive = 0.110/pperm = 0.014) and NKX2-1 (rs999460) (βrecessive = -0.176/pperm = 0.015). Ten BW-significant models of interSNPs interactions (pperm ≤ 0.001) were identified for 20 polymorphisms. SNPs rs7538038 KISS1, rs713586 RBJ, rs12324955 FTO and rs713586 RBJ-rs12324955 FTO two-locus interaction were included in the largest number of BW-associated models (30% models each). BW-associated AAM-linked 22 SNPs and 350 proxy loci were functionally related to 49 genes relevant to pathways such as the hormone biosynthesis/process and female/male gonad development. In conclusion, maternal AMM-related genes polymorphism is associated with the offspring BW.
| S-EPMC10381708 | biostudies-literature
Project description:BackgroundEvidence suggests that in utero exposure to undernutrition and overnutrition might affect adiposity in later life. Epigenetic modification is suggested as a plausible mediating mechanism.MethodsWe used multivariable linear regression and a negative control design to examine offspring epigenome-wide DNA methylation in relation to maternal and offspring adiposity in 1018 participants.ResultsCompared with neonatal offspring of normal weight mothers, 28 and 1621 CpG sites were differentially methylated in offspring of obese and underweight mothers, respectively [false discovert rate (FDR)-corrected P-value < 0.05), with no overlap in the sites that maternal obesity and underweight relate to. A positive association, where higher methylation is associated with a body mass index (BMI) outside the normal range, was seen at 78.6% of the sites associated with obesity and 87.9% of the sites associated with underweight. Associations of maternal obesity with offspring methylation were stronger than associations of paternal obesity, supporting an intrauterine mechanism. There were no consistent associations of gestational weight gain with offspring DNA methylation. In general, sites that were hypermethylated in association with maternal obesity or hypomethylated in association with maternal underweight tended to be positively associated with offspring adiposity, and sites hypomethylated in association with maternal obesity or hypermethylated in association with maternal underweight tended to be inversely associated with offspring adiposity.ConclusionsOur data suggest that both maternal obesity and, to a larger degree, underweight affect the neonatal epigenome via an intrauterine mechanism, but weight gain during pregnancy has little effect. We found some evidence that associations of maternal underweight with lower offspring adiposity and maternal obesity with greater offspring adiposity may be mediated via increased DNA methylation.
| S-EPMC4588865 | biostudies-literature
Project description:The effect of preconception drinking by the mother on the life-long health outcomes of her children is not known, and therefore, in this study using an animal model, we determined the impact of preconception alcohol drinking of the mother on offspring stress response during adulthood. In our preconception alcohol exposure model, adult female rats were fed with 6.7% alcohol in their diet for 4 weeks, went without alcohol for 3 weeks and were bred to generate male and female offspring. Preconception alcohol-exposed offsprings' birth weight, body growth, stress response, anxiety-like behaviors, and changes in stress regulatory gene and protein hormone levels were evaluated. In addition, roles of epigenetic mechanisms in preconception alcohol effects were determined. Alcohol feeding three weeks prior to conception significantly affected pregnancy outcomes of female rats, with respect to delivery period and birth weight of offspring, without affecting maternal care behaviors. Preconception alcohol negatively affected offspring adult health, producing an increased stress hormone response to an immune challenge. In addition, preconception alcohol was associated with changes in expression and methylation profiles of stress regulatory genes in various brain areas. These changes in stress regulatory genes were normalized following treatment with a DNA methylation blocker during the postnatal period. These data highlight the novel possibility that preconception alcohol affects the inheritance of stress-related diseases possibly by epigenetic mechanisms.
| S-EPMC5026748 | biostudies-literature
Project description:BackgroundPerfluoroalkyl substances (PFASs) are widespread, bioaccumulating, and persistent and show placental transfer. Emerging research indicates associations between prenatal exposure and low birth weight. The aim of this study was to assess the associations between first trimester exposure to PFASs and birth weight (BW) in the Swedish Environmental, Longitudinal, Mother and child, Asthma and allergy (SELMA) study and examine whether associations differ between girls and boys.MethodsEight PFASs were analyzed in maternal serum (median: 10 weeks of pregnancy). Associations between prenatal PFAS exposure and birth outcomes with BW, BW for gestational age, and birth small for gestational age (SGA) were assessed in 1533 infants, adjusted for potential confounders and stratified by sex.ResultsIncreased maternal perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroundecanoic acid (PFUnDA) were associated with lower BW, lower BW for gestational age, and SGA birth. Associations were significant only in girls, where prenatal exposure in the upper quartile was associated with a 93-142-g lower BW when compared with that of the lowest quartile exposure. The associations were not mediated by effects on gestational age.ConclusionsWe found associations between prenatal exposure for five different PFASs and birth weight, with more pronounced associations in girls than in boys.
| S-EPMC7196936 | biostudies-literature
Project description:BackgroundSparse data are available on the relationship between prenatal exposures and asthma during later childhood. In a longitudinal study of adolescents and their mothers, we examined the association of (i) maternal prepregnancy body mass index (BMI) and (ii) gestational weight gain (GWG), with incidence of allergic and nonallergic asthma in offspring.MethodsAnalyses were conducted using data from 12 963 children aged 9-14 years at enrolment in the Growing Up Today Study, and their mothers, who are participants in the Nurses' Health Study II. Physician-diagnosed asthma and allergies were assessed by questionnaires sent regularly to participants and their mothers. Logistic regression was used to evaluate associations of maternal BMI and GWG with offspring asthma, overall and by subtype.ResultsPhysician-diagnosed asthma during childhood or adolescence was reported by 2694 children (21%). Maternal prepregnancy overweight (OR: 1.19, 95% CI: 1.03-1.38) and obesity (1.34, 1.08-1.68) were associated with offspring asthma. In asthma subtype analyses, the association was seen only for asthma onset before age 12 years. Moreover, the association of maternal obesity with nonallergic asthma was observed in boys (2.39, 1.40-4.09) and not in girls (0.96, 0.50-1.85; Pinteraction = 0.03); the opposite pattern was suggested for allergic asthma. With regard to GWG, an association was suggested between gains of <15 lb and higher risk of offspring asthma (1.28, 0.98-1.66), without clear allergy- or sex-related patterns.ConclusionThe relation of several prenatal factors to risk of childhood asthma supports the early origins hypothesis for asthma. The observed allergy- and sex-specific patterns suggest multiple etiologic pathways.
| S-EPMC4975656 | biostudies-literature