The rising prevalence of overweight and obesity is a worldwide public health challenge. Pregnancy and beyond is a potentially important window for future weight gain in women. We investigated associations between maternal adherence to the New Nordic diet (NND) during pregnancy and maternal BMI trajectories from delivery to 8 years post delivery. Data are from the Norwegian Mother and Child Cohort. Pregnant women from all of Norway were recruited between 1999 and 2008, and 55 056 are included in the present analysis. A previously constructed diet score, NND, was used to assess adherence to the diet. The score favours intake of Nordic fruits, root vegetables, cabbages, potatoes, oatmeal porridge, whole grains, wild fish, game, berries, milk and water. Linear spline multi-level models were used to estimate the association. We found that women with higher adherence to the NND pattern during pregnancy had on average lower post-partum BMI trajectories and slightly less weight gain up to 8 years post delivery compared with the lower NND adherers. These associations remained after adjustment for physical activity, education, maternal age, smoking and parity (mean diff at delivery (high v. low adherers): -0·3 kg/m2; 95 % CI -0·4, -0·2; mean diff at 8 years: -0·5 kg/m2; 95 % CI -0·6, -0·4), and were not explained by differences in energy intake or by exclusive breast-feeding duration. Similar patterns of associations were seen with trajectories of overweight/obesity as the outcome. In conclusion, our findings suggest that the NND may have beneficial properties to long-term weight regulation among women post-partum.
Infections in early life have been linked to type 1 diabetes (T1D) risk, but no previous study has comprehensively analysed exposure to antibiotics, acetaminophen and infections during pregnancy and early childhood in relation to offspring risk of T1D.
Participants in the Norwegian Mother and Child Cohort Study (n?=?114 215 children, of whom 403 children were diagnosed with T1D) reported infections and medication use through repeated questionnaires from pregnancy until the children were 18?months old. Adjusted hazard ratios (aHR) for offspring T1D were estimated through Cox regression adjusted for child's sex, maternal age and parity, maternal T1D, smoking in pregnancy, education level, pre-pregnancy body mass index (BMI) and birthweight. Antibiotic use was also analysed in a population-based register cohort of 541 036 children of whom 836 developed T1D.
Hospitalization for gastroenteritis during the first 18?months of life was associated with increased risk (aHR 2.27, 95% CI 1.21 - 4.29, P?=?0.01) of T1D. Childhood infections not requiring hospitalization, or any kind of maternal infection during pregnancy, did not predict offspring risk of T1D. Antibiotic or acetaminophen use in pregnancy, or child`s use in early childhood, was not associated with risk of T1D.
Our study, which is population-based and the largest of its kind, did not find support for general early life infections, infection frequency or use of antibiotics or acetaminophen to play a major role in childhood T1D. Hospital admission for gastroenteritis was associated with T1D risk, but must be interpreted cautiously due to scarcity of cases.
Experiencing a stillbirth can be a potent stressor for psychological distress in the subsequent pregnancy and possibly after the subsequent birth. The impact on women's relationship with her partner in the subsequent pregnancy and postpartum remains uncertain. The objectives of the study were 1) To investigate the prevalence of anxiety and depression in the pregnancy following stillbirth and assess gestational age at stillbirth and inter-pregnancy interval as individual risk factors. 2) To assess the course of anxiety, depression and satisfaction with partner relationship up to 3 years after the birth of a live-born baby following stillbirth.
This study is based on data from the Norwegian Mother and Child Cohort Study, a population-based pregnancy cohort. The sample included 901 pregnant women: 174 pregnant after a stillbirth, 362 pregnant after a live birth and 365 previously nulliparous. Anxiety and depression were assessed by short-form subscales of the Hopkins Symptoms Checklist, and relationship satisfaction was assessed by the Relationship Satisfaction Scale. These outcomes were measured in the third trimester of pregnancy and 6, 18 and 36 months postpartum. Logistic regression models were applied to study the impact of previous stillbirth on depression and anxiety in the third trimester of the subsequent pregnancy and to investigate gestational age and inter-pregnancy interval as potential risk factors.
Women pregnant after stillbirth had a higher prevalence of anxiety (22.5%) and depression (19.7%) compared with women with a previous live birth (adjusted odds ratio (aOR) 5.47, 95% confidence interval (CI) 2.90-10.32 and aOR 1.91, 95% CI 1.11-3.27) and previously nulliparous women (aOR 4.97, 95% CI 2.68-9.24 and aOR 1.91, 95% CI 1.08-3.36). Gestational age at stillbirth (>?30 weeks) and inter-pregnancy interval?
Hans Christian Andersen Children's Hospital, Odense University Hospital, Odense, Denmark; Department of Clinical Research, University of Southern Denmark, Odense, Denmark. Electronic address: email@example.com.
The intestinal microbiota is believed to be involved in the pathogenesis of celiac disease, in addition to genetic variants and dietary gluten. The gut microbiota is strongly influenced by systemic antibiotics-especially in early life. We explored the association between exposure to a systemic antibiotic in the first year of life and risk of diagnosed celiac disease.
We performed an observational nationwide register-based cohort study. We included all children born in Denmark from 1995 through 2012 or Norway from 2004 through 2012. Children born in Denmark were followed until May 8, 2015 (age at end of follow-up was 2.3-20.3 years) and children born in Norway were followed until December 31, 2013 (age at end of follow-up was 1-10 years). We collected medical information from more than 1.7 million children, including 3346 with a diagnosis of celiac disease. Exposure to systemic antibiotics was defined as a dispensed systemic antibiotic in the first year of life.
Exposure to systemic antibiotics in the first year of life was positively associated with diagnosed celiac disease in the Danish and Norwegian cohorts (pooled odds ratio 1.26, 95% confidence interval 1.16-1.36). We found a dose-dependent relation between an increasing number of dispensed antibiotics and the risk of celiac disease (pooled odds ratio for each additional dispensed antibiotic 1.08, 95% confidence interval 1.05-1.11). No specific type of antibiotic or age period within the first year of life was prominent. Adjustment for hospital admissions with an infectious disease in the first year of life did not change the estimates; adjustment for the number of maternally reported infections in the child in 2 large sub-cohorts decreased the association slightly (pooled odds ratio 1.18, 95% confidence interval 0.98-1.39).
In a nationwide study of children in Denmark and Norway, we found exposure to systemic antibiotics in the first year of life to be associated with a later diagnosis of celiac disease. These findings indicate that childhood exposure to systemic antibiotics could be a risk factor for celiac disease.
Prenatal maternal psychosocial stress might influence the development of childhood asthma. Evaluating paternal psychosocial stress and conducting a sibling comparison could provide further insight into the role of unmeasured confounding. We examined the associations of parental psychosocial stress during and after pregnancy with asthma at age 7 years in the Norwegian Mother and Child Cohort Study (n = 63,626; children born in 2000-2007). Measures of psychosocial stress included lifetime major depressive symptoms, current anxiety/depression symptoms, use of antidepressants, anxiolytics, and/or hypnotics, life satisfaction, relationship satisfaction, work stress, and social support. Childhood asthma was associated with maternal lifetime major depressive symptoms (adjusted relative risk (aRR) = 1.19, 95% confidence interval (CI): 1.09, 1.30), in addition to symptoms of anxiety/depression during pregnancy (aRR = 1.17, 95% CI: 1.06, 1.29) and 6 months after delivery (aRR = 1.17, 95% CI: 1.07, 1.28). Maternal negative life events during pregnancy (aRR = 1.10, 95% CI: 1.06, 1.13) and 6 months after delivery (aRR = 1.14, 95% CI: 1.11, 1.18) were also associated with asthma. These associations were not replicated when evaluated within sibling groups. There were no associations with paternal psychosocial stress. In conclusion, maternal anxiety/depression and negative life events were associated with offspring asthma, but this might be explained by unmeasured maternal background characteristics that remain stable across deliveries.
Studies on medication safety in pregnancy often rely on an oversimplification of medication use into exposed or non-exposed, without considering intensity and timing of use in pregnancy, or concomitant medication use. This study uses paracetamol in pregnancy as the motivating example to introduce a method of clustering medication exposures longitudinally throughout pregnancy. The aim of this study was to use hierarchical cluster analysis (HCA) to better identify clusters of medication exposure throughout pregnancy.
Data from the Norwegian Mother and Child Cohort Study was used to identify subclasses of women using paracetamol during pregnancy. HCA with customized distance measure was used to identify clusters of medication exposures in pregnancy among children at 18 months.
The pregnancies in the study (N = 9 778) were grouped in 5 different clusters depending on their medication exposure profile throughout pregnancy.
Using HCA, we identified and described profiles of women exposed to different medications in combination with paracetamol during pregnancy. Identifying these clusters allows researchers to define exposure in ways that better reflects real-world medication usage patterns. This method could be extended to other medications and used as pre-analysis for identifying risks associated with different profiles of exposure.
Cites: Int J Epidemiol. 2006 Oct;35(5):1146-50 PMID 16926217
Cites: Ann Transl Med. 2016 Mar;4(5):91 PMID 27047950
INSERM, UMR1153 Epidemiology and Biostatistics Sorbonne Paris Cité Center (CRESS), Early determinants of the child's health and development Team (ORCHAD), Paris F-75014, France; Paris Descartes University, Paris, France. Electronic address: firstname.lastname@example.org.
Prenatal acrylamide exposure has been negatively associated with fetal growth but the association with child growth is unknown.
We studied the association between prenatal acrylamide exposure and child postnatal growth up to 8?years in the Norwegian Mother and Child Cohort Study (MoBa).
In 51,952 mother-child pairs from MoBa, acrylamide intake during pregnancy was estimated by combining maternal food intake with food concentrations of acrylamide. Mothers reported their child's weight and length/height up to 11 times between 6?weeks and 8?years. Weight and height growth trajectories were modelled using Jenss-Bayley's growth model. Logistic regression models were used to study the association with overweight/obese status at 3, 5 and 8?years, as identified using the International Obesity Task Force cut-offs. Linear mixed-effect models were used to explore associations with overall growth.
At 3?years, the adjusted odds ratios (95% Confidence Intervals (CI)) of being overweight/obese were 1.10 (1.02, 1.20), 1.12 (1.04, 1.22) and 1.21 (1.11, 1.31) by increasing prenatal acrylamide exposure quartile. Similar dose-response associations were found at 5 and 8?years. Acrylamide intake during pregnancy was associated with higher weight growth velocity in childhood. Children exposed at the highest level had 22?g (95% CI: 8, 37), 57?g (95% CI: 32, 81), and 194?g (95% CI: 110, 278) higher weight at 0.5, 2, and 8?years, respectively, compared to their low exposed peers.
Children prenatally exposed to acrylamide in the highest quartile experienced a moderate increase in weight growth velocity during early childhood that resulted in a moderately increased prevalence of overweight/obesity compared to peers in the lowest quartile. Our study is the first to link prenatal acrylamide exposure and postnatal growth.
We examined the association between pregnancy and life-course lipid trajectories. Linked data from the Nord-Trøndelag Health Study and the Medical Birth Registry of Norway yielded 19,987 parous and 1,625 nulliparous women. Using mixed-effects spline models, we estimated differences in nonfasting lipid levels from before to after first birth in parous women and between parous and nulliparous women. HDL cholesterol (HDL-C) dropped by -4.2 mg/dl (95% CI: -5.0, -3.3) from before to after first birth in adjusted models, a 7% change, and the total cholesterol (TC) to HDL-C ratio increased by 0.18 (95% CI: 0.11, 0.25), with no change in non-HDL-C or triglycerides. Changes in HDL-C and the TC/HDL-C ratio associated with pregnancy persisted for decades, leading to altered life-course lipid trajectories. For example, parous women had a lower HDL-C than nulliparous women at the age of 50 years (-1.4 mg/dl; 95% CI: -2.3, -0.4). Adverse changes in lipids were greatest after first birth, with small changes after subsequent births, and were larger in women who did not breastfeed. Findings suggest that pregnancy is associated with long-lasting adverse changes in HDL-C, potentially setting parous women on a more atherogenic trajectory than prior to pregnancy.
Preeclampsia is thought to originate during placentation, with incomplete remodelling and perfusion of the spiral arteries leading to reduced placental vascular capacity. Nitric oxide (NO) and carbon monoxide (CO) are powerful vasodilators that play a role in the placental vascular system. Although family clustering of preeclampsia has been observed, the existing genetic literature is limited by a failure to consider both mother and child.
We conducted a nested case-control study within the Norwegian Mother and Child Birth Cohort of 1545 case-pairs and 995 control-pairs from 2540 validated dyads (2011 complete pairs, 529 missing mother or child genotype). We selected 1518 single-nucleotide polymorphisms (SNPs) with minor allele frequency >5% in NO and CO signalling pathways. We used log-linear Poisson regression models and likelihood ratio tests to assess maternal and child effects.
One SNP met criteria for a false discovery rate Q-value
A statistical mediation model was developed within a twin design to investigate the etiology of alcohol use disorder (AUD). Unlike conventional statistical mediation models, this biometric mediation model can detect unobserved confounding. Using a sample of 1410 pairs of Norwegian twins, we investigated specific hypotheses that DSM-IV personality-disorder (PD) traits mediate effects of childhood stressful life events (SLEs) on AUD, and that adulthood SLEs mediate effects of PDs on AUD. Models including borderline PD traits indicated unobserved confounding in phenotypic path coefficients, whereas models including antisocial and impulsive traits did not. More than half of the observed effects of childhood SLEs on adulthood AUD were mediated by adulthood antisocial and impulsive traits. Effects of PD traits on AUD 5?10 years later were direct rather than mediated by adulthood SLEs. The results and the general approach contribute to triangulation of developmental origins for complex behavioral disorders.