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Objectives: To investigate the association between maternal early pregnancy body mass index (BMI) and offspring bipolar disorder (BPD). Methods: We conducted a nationwide cohort study among 1,507,056 non‐malformed singleton live‐births in Sweden born 1983–2004. Using national registries with prospectively recorded information, we followed participants for a BPD diagnosis from ages 13 to up to 35 years. We compared BPD risks by early pregnancy BMI using hazard ratios (HR) with 95% confidence intervals (CI) from adjusted Cox models. We also conducted sibling‐controlled analyses among 874,047 full siblings. Results: There were 9970 BPD diagnoses. Risk of BPD was 0.72% through 25 years of age. Maternal early pregnancy BMI was positively associated with offspring BPD risk. Compared with normal BMI (18.5–24.9), adjusted HR (95% CI) for overweight (BMI 25–29.9), obesity grade 1 (BMI 30–34.9), and obesity grades 2–3 (BMI ≥35) were 1.08 (1.02, 1.15), 1.26 (1.14, 1.40), and 1.31 (1.07, 1.60), respectively. Adjusted HR per unit BMI was 1.015 (95% CI 1.009, 1.021). A similar trend was observed among siblings. Pregnancy and neonatal complications did not substantially mediate the association between maternal obesity (BMI ≥30) and offspring BPD. Conclusions: Maternal BMI ≥25 is associated with offspring BPD risk in a dose–response manner. [ABSTRACT FROM AUTHOR]

The International Collaboration for Autism Registry Epidemiology (iCARE) is the first multinational research consortium (Australia, Denmark, Finland, Israel, Norway, Sweden, USA) to promote research in autism geographical and temporal heterogeneity, phenotype, family and life course patterns, and etiology. iCARE devised solutions to challenges in multinational collaboration concerning data access security, confidentiality and management. Data are obtained by integrating existing national or state-wide, population-based, individual-level data systems and undergo rigorous harmonization and quality control processes. Analyses are performed using database federation via a computational infrastructure with a secure, web-based, interface. iCARE provides a unique, unprecedented resource in autism research that will significantly enhance the ability to detect environmental and genetic contributions to the causes and life course of autism.

Objectives: To investigate associations of neonatal characteristics and pregnancy complications with bipolar disorder (BPD) in offspring. Methods: We conducted a nationwide cohort study among 2,059,578 non‐malformed singleton live‐births in Sweden born 1983–2004. Using national registries with prospectively recorded information, we followed participants for a BPD diagnosis from 13 up to 34 years of age. We compared BPD risks between exposure categories using hazard ratios (HR) with 95% confidence intervals (CI) from adjusted Cox models. We also conducted sibling‐controlled analyses among 1,467,819 full siblings. Results: There were 14,998 BPD diagnoses. Risk of BPD was 0.74% through 25 years of age. Very/extremely preterm birth (22 to 31 weeks) was related to increased BPD HRs in sibling‐controlled analyses; compared with a gestational age of 37 weeks, adjusted HR (95% CI) for 31, 28, and 22 weeks were, respectively, 1.31 (0.99, 1.74), 2.09 (1.15, 3.79), and 5.74 (1.15, 28.63). Spontaneous but not medically indicated very/extremely preterm birth was associated with increased risk. Compared with vaginal birth, caesarean section birth was associated with 1.20 (1.08, 1.33) and 1.58 (1.06, 2.36) times higher BPD risk in general and sibling cohorts, respectively. Small‐for‐gestational age (SGA) birth was related to increased BPD HRs in general cohort and sibling analyses (HRs [95% CI] were 1.22 [1.06, 1.39] and 1.68 [1.13, 2.50], respectively); only term SGA was associated with increased risk. Head circumference‐for‐gestational age, gestational diabetes, preeclampsia, and placental abruption were not associated with BPD. Conclusions: Very/extremely preterm birth, caesarean birth, and SGA are related to BPD incidence. [ABSTRACT FROM AUTHOR]

We investigated the relationships between syndromic manifestations of defective placentation and the incidence of intellectual disability (ID) in offspring by conducting a population-based cohort study of 1,581,200 nonmalformed, live singleton infants born in Sweden between 1998 and 2014. Exposures were: 1) placental abruption, 2) preterm preeclampsia (<34 weeks of gestation), 3) preeclampsia combined with infant being small for gestational age (SGA) at birth, and 4) spontaneous preterm birth. The outcome was an ID diagnosis after 3 years of age. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for each syndrome using Cox regression and robust variances. There were 9,451 children with ID (5.5 per 10,000 child-years). ID incidence rates increased with placental abruption (HR = 2.8, 95% CI: 2.3, 3.5), preterm preeclampsia (HR = 3.7, 95% CI: 2.9, 4.7), preeclampsia combined with SGA (HR = 3.3, 95% CI: 2.6, 4.1), and spontaneous preterm birth (for 32–36 and 22–31 weeks, respectively, HR = 1.6 (95% CI: 1.4, 1.8) and 5.2 (95% CI: 4.3, 6.2)). The same pattern of results was evident in sibling-controlled analyses among 1,043,158 full siblings. The strength of associations increased with ID severity. Preterm birth only partly explained the associations of placental abruption, preeclampsia, or SGA with ID. We conclude that defective placentation is related to increased incidence of ID in the offspring. [ABSTRACT FROM AUTHOR]

Aim: The aim of this study was to investigate preterm birth, small‐for‐gestational age (SGA), preeclampsia and placental abruption in relation to attention‐deficit/hyperactivity disorder (ADHD) in offspring. Methods: We conducted a population‐based cohort study among non‐malformed live‐born singleton children in Sweden born during 2002–2014. Using national registries with recorded information, we followed 1,212,201 children for an ADHD diagnosis from 3 to 15 years. We compared ADHD rates between exposure categories using adjusted hazard ratios (HR) with 95% confidence intervals (CI) from Cox proportional hazards models. We also conducted sibling‐controlled analyses among 751,464 full siblings. Results: There were 27,665 ADHD diagnoses in the cohort. Compared with term birth (≥37 weeks), adjusted HR (95% CI) for ADHD increased with decreasing gestational age: 1.18 (1.11, 1.25), 1.61 (1.37, 1.89) and 2.79 (2.23, 3.49) for 32–36 weeks, 28–31 weeks and 22–27 weeks. Both spontaneous and medically indicated preterm birth were associated with ADHD. SGA was related to 1.62 (1.49, 1.77) times higher ADHD incidence. Preeclampsia, but not placental abruption, was associated with ADHD. Sibling‐controlled analyses showed similar results. Preterm birth did not fully explain the associations of SGA or preeclampsia with ADHD. Conclusion: Preterm birth, SGA and preeclampsia are related to ADHD incidence in offspring. [ABSTRACT FROM AUTHOR]

Defective placentation underlies diverse syndromic manifestations that could affect brain development including: (1) placental abruption, (2) term preeclampsia with a small-for-gestational age (SGA) infant, (3) preterm preeclampsia, and (4) spontaneous preterm birth. We investigated the relations between these defective placentation syndromes and the incidence of Autism Spectrum Disorder (ASD) in offspring. We conducted a population-based cohort study of 1,645,455 non-malformed singleton infants born in Sweden 2000–2016 who were followed for up to 17 years using national registers. We compared ASD rates for children prenatally exposed and unexposed to defective placentation syndromes with use of adjusted hazard ratios (HR) with 95% confidence intervals (CI) from Cox regression. We also conducted sibling-controlled analyses among 1,092,132 full siblings. The association of the syndromes with ASD independent of preterm birth was estimated in mediation analyses. There were 23,810 cases of ASD. In both general cohort and sibling analyses, adjusted HRs (95% CI) of ASD were increased in children of mothers with term preeclampsia combined with SGA [1.5 (1.3, 1.9) and 1.9 (1.1, 3.3), respectively], preterm preeclampsia < 34 weeks [1.8 (1.4, 2.2) and 4.2 (2.1, 8.5), respectively], and spontaneous very or extremely preterm birth (≤ 31 weeks) [2.6 (2.2, 3.0) and 2.4 (1.5, 3.8), respectively]. Placental abruption was associated with increased HR of ASD in general cohort analysis only. The association between preeclampsia and ASD was not fully explained by preterm birth. In conclusion, syndromes linked to defective placentation are associated with increased incidence of ASD in the offspring. [ABSTRACT FROM AUTHOR]

The article discusses a population-based cohort study which determined the effect of low birth weight with increased risk for adult schizophrenia or other adult mental illnesses. In the population-based cohort research conducted in Sweden and Denmark, two phases of analyses were made using the Stata version 10 software and the SAS version 9.1 software. Results show that birth weight is somehow linked with adult mental disorder.