The use of oral contraceptive before pregnancy and breastfeeding duration: A cross-sectional study with retrospective ascertainment

<p>Abstract</p> <p>Background</p> <p>Various studies have identified risk factors associated with decreased breastfeeding duration. The aim of this study was to investigate whether there is an association between oral contraceptive (OC) use before pregnancy and breastfeeding duration.</p> <p>Methods</p> <p>In 1994/95, as part of a 3-year epidemiologic follow-up study of school children, reproductive interviews were conducted with their mothers. The study population consists of 663 women residing in Hesse, Central Germany; 575 provided information on their reproductive history. The interview included retrospective ascertainment of OC use, its timing before pregnancy, and duration of breastfeeding. To estimate its effect on duration of breastfeeding, survival analysis was applied controlling for maternal age, socio-demographic characteristics, smoking during pregnancy, age at menarche, planning of the pregnancy and birth order. Hazard ratios and median breastfeeding duration were estimated.</p> <p>Results</p> <p>The mean age of the women at delivery was 27.3 years. Among participants, 34.9% had high school education or less, 10.4% had more than 2 children, and 30.1% smoked during pregnancy. In total, oral contraceptive use in the 12 months before conception was reported by 40.4% of the women, within 3 months of conception by 18.4%. 81.4% (468/575) of women initiated breastfeeding. Compared to those who did not use OC in the 12 months preceding pregnancy, mothers who used OC during the 3 months before conception had a shorter duration of breastfeeding (HR = 1.29; 95% CI: 1.03, 1.61), as did mothers who stopped OC use 4–12 months before conception (HR = 1.27, 95% CI: 1.02, 1.58). Smoking during pregnancy and lower education were also significantly associated with shorter duration of breastfeeding.</p> <p>Conclusion</p> <p>The results suggest that OC use during the 12 months prior to conception may affect breastfeeding duration. These findings may be due to the endocrine disrupting effect of OC. Alternatively, both OC use and shorter duration of breastfeeding may represent lifestyle-related conditions.</p

Body Burden of Dichlorodiphenyl Dichloroethene (DDE) and Childhood Pulmonary Function

Longitudinal studies have shown that early life exposure to dichlorodiphenyl dichloroethene (DDE) can lead to growth reduction during childhood and adolescence. In addition, DDE exposure has been linked to respiratory tract infections and an increased risk of asthma in children. Our aim was to understand the relationships between DDE exposure and pulmonary function in children, and, particularly, whether associations are mediated by the height of the children. We used data from an environmental epidemiologic study conducted in central Germany in children aged 8-10 years. The pulmonary function (forced vital capacity, FVC, and forced expiratory volume in one second, FEV1) were measured in three consecutive years. Blood DDE levels were measured at 8 and 10 years. We used linear mixed models for repeated measurements and path analyses to assess the association between blood levels of DDE and pulmonary function measurements. All models were adjusted for confounders. Linear mixed approaches and modelling concurrent effects showed no significant associations. The path analytical models demonstrated that DDE measured at eight years had significant, inverse, indirect, and total effects on FVC at ten years (n = 328; −0.18 L per μg/L of DDE) and FEV1 (n = 328; −0.17 L per μg/L of DDE), mediated through effects of DDE on height and weight. The DDE burden reduces pulmonary function through its diminishing effects on height and weight in children. Further studies are required to test these associations in other samples, preferably from a region with ongoing, high DDT application

Sex Differences in the Association of Sibship Size and Position in Sibship with Lipid Profile During Adolescence: A Cross-Sectional Study

Background. Epidemiologic studies have reported associations of sibship size and position of the child in the sibship with multiple health outcomes, including adiposity and diabetes. However, little is known about sibling effects on lipids. Hence, this study sought to evaluate associations of the number of total, older, and younger siblings with lipid profile among adolescents. Methods. In a cross-sectional study among high school students aged 14 to 19 years, lipid levels were measured in capillary blood. Parents reported the number of siblings (total, older, and younger). Geometric means of lipids were calculated, and linear regression was used to estimate the ratio of geometric means (RoGM) and 95% confidence intervals (CI). Analyses were sex stratified. Results. Of the total study sample (n = 1,584), 758 (47.9%) were boys and 826 (52.1%) were girls, with median age of 16.0 years. Total cholesterol (TC) was lower by 8% (adjusted-RoGM = 0.92, 95% CI: 0.88–0.96) among boys with ≥3 older siblings compared to those with no older siblings. Similarly, boys with ≥3 younger sibling compared to those with no younger siblings had reduced TC by 7% (adjusted-RoGM = 0.93, 0.87–0.99). Moreover, an increased number of total siblings (≥4 vs. 0/1: adjusted-RoGM = 0.80, 0.67–97) and older siblings (≥3 vs. 0: adjusted-RoGM = 0.90, 0.82–0.98) were associated with reduced low-density lipoprotein cholesterol (LDL-C) among boys. Similarly, lower levels of triglycerides (TG) were seen among boys with ≥3 older siblings compared to those with no older siblings (adjusted-RoGM = 0.87, 0.78–0.96). A higher number of younger siblings was associated with increased high-density lipoprotein cholesterol (HDL-C) among boys (≥3 vs. 0: adjusted-RoGM = 1.08, 1.01–1.17). Sibship characteristics were not associated with lipids among girls. Conclusions. Increased number of total, older, and younger siblings were associated with favorable lipid profiles among adolescent boys, but not girls. Mechanisms underlying these associations need further investigations

Identifying heterogeneous transgenerational DNA methylation sites via clustering in beta regression

This paper explores the transgenerational DNA methylation pattern (DNA methylation transmitted from one generation to the next) via a clustering approach. Beta regression is employed to model the transmission pattern from parents to their offsprings at the population level. To facilitate this goal, an expectation maximization algorithm for parameter estimation along with a BIC criterion to determine the number of clusters is proposed. Applying our method to the DNA methylation data composed of 4063 CpG sites of 41 mother–father-infant triads, we identified a set of CpG sites in which DNA methylation transmission is dominated by fathers, while at a large number of CpG sites, DNA methylation is mainly maternally transmitted to the offspring

An efficient approach to screening epigenome-wide data

Screening cytosine-phosphate-guanine dinucleotide (CpG) DNA methylation sites in association with some covariate(s) is desired due to high dimensionality. We incorporate surrogate variable analyses (SVAs) into (ordinary or robust) linear regressions and utilize training and testing samples for nested validation to screen CpG sites. SVA is to account for variations in the methylation not explained by the specified covariate(s) and adjust for confounding effects. To make it easier to users, this screening method is built into a user-friendly R package, ttScreening, with efficient algorithms implemented. Various simulations were implemented to examine the robustness and sensitivity of the method compared to the classical approaches controlling for multiple testing: the false discovery rates-based (FDR-based) and the Bonferroni-based methods. The proposed approach in general performs better and has the potential to control both types I and II errors. We applied ttScreening to 383,998 CpG sites in association with maternal smoking, one of the leading factors for cancer risk

Effects of phthalate exposure on asthma may be mediated through alterations in DNA methylation

Background: phthalates may increase the asthma risk in children. Mechanisms underlying this association remain to be addressed. This study assesses the effect of phthalate exposures on epigenetic changes and the role of epigenetic changes for asthma. In the first step, urine and blood samples from 256 children of the Childhood Environment and Allergic diseases Study (CEAS) were analyzed. Urine 5OH-MEHP levels were quantified as an indicator of exposure, and asthma information was collected. DNA methylation (DNA-M) was measured by quantitative PCR. In the screening part of step 1, DNA-M of 21 potential human candidate genes suggested by a toxicogenomic data were investigated in 22 blood samples. Then, in the testing part of step 1, positively screened genes were tested in a larger sample of 256 children and then validated by protein measurements. In step 2, we replicated the association between phthalate exposure and gene-specific DNA-M in 54 children in the phthalate contaminated food event. In step 3, the risk of DNA-M for asthma was tested in 256 children from CEAS and corroborated in 270 children from the Isle of Wight (IOW) birth cohort. Results: differential methylation in three genes (AR, TNF?, and IL-4) was identified through screening. Testing in 256 children showed that methylation of the TNF? gene promoter was lower when children had higher urine 5OH-MEHP values (??=??0.138, P?=?0.040). Functional validation revealed that TNF? methylation was inversely correlated with TNF? protein levels (??=??0.18, P?=?0.041). In an additional sample of 54 children, we corroborated that methylation of the TNF? gene promoter was lower when urine 5OH-MEHP concentrations were higher. Finally, we found that a lower methylation of 5?CGI region of TNF? was associated with asthma in 256 CEAS children (OR?=?2.15, 95% CI?=?1.01 to 4.62). We replicated this in 270 children from the IOW birth cohort study. Methylation of the CpG site cg10717214 was negatively associated with asthma, when children had ‘AA’ or ‘AG’ genotype of the TNF? single nucleotide rs1800610. Conclusions: effects of phthalate exposure on asthma may be mediated through alterations in DNA methylatio

DDE and PCB serum concentration in maternal blood and their adult female offspring

Background: Dichlorodiphenyl dichloroethylene (DDE) and polychlorinated biphenyls (PCBs) can be passed from mother to offspring through placental transfer or breast feeding. Unknown is whether maternal levels can predict concentrations in adult offspring. Objectives: To test the association between maternal blood levels of DDE and PCBs and adult female offspring levels of these compounds using data from the Michigan Fisheaters’Cohort. Methods: DDE and PCB concentrations were determined in 132 adult daughters from 84 mothers. Prenatal exposures were estimated based on maternal DDE and PCB serum levels measured between 1973 and 1991. Levels in adult daughters were regressed on maternal and estimated prenatal exposure levels, adjusting for potential confounders using linear mixed models. Confounders included daughter’s age, birth order, birth weight, number of pregnancies, the length of time the daughter was breast-fed, the length of time the daughter breast-fed her own children, last year fish-eating status, body mass index, and lipid weight. Results: The median age of the participants was 40.4 years (range 18.4 to 65.4, 5–95 percentiles 22.5-54.6%, respectively). Controlling for confounders and intra-familial associations, DDE and PCB concentrations in adult daughters were significantly positively associated with estimated prenatal levels and with maternal concentrations. The proportion of variance in the adult daughters’ organochlorine concentrations explained by the maternal exposure levels is approximately 23% for DDE and 43% for PCBs. The equivalent of a median of 3.67 μg/L prenatal DDE and a median of 2.56 μg/L PCBs were 15.64 and 10.49 years of fish consumption, respectively. When controlling for effects of the shared environment (e.g., fish diet) by using a subsample of paternal levels measured during the same time frames (n=53 and n=37), we determined that the direct maternal transfer remains important. Conclusions: Estimated intrauterine DDE and PCB levels predicted concentrations in adult female offspring 40 years later. Interpretation of adverse health effects from intrauterine exposures of persistent pollutants may need to consider the sustained impact of maternal DDE and PCB levels found in their offspring