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Background: Low educational attainment in parents is associated with child psychopathology. It is not clear whether the associations are due to risk factors that family members share or due to effects of maternal or paternal education on the offspring. We investigate whether associations between maternal and paternal educational attainment and child symptoms of attention deficit/hyperactivity disorder (ADHD), depression, and academic problems are due to shared genetic factors, shared family environmental factors, or effects of the parental phenotype educational attainment itself., Methods: This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). The sample comprised 34,958 children (17,128 girls) in 28,372 extended-family units. We used data from related nuclear families linked by siblings in the parent generation. We applied a quasi-experimental extended children-of-twins design that included siblings in both generations and took account of nonrandom mating by including partners. Educational attainment was self-reported by mothers and fathers. Mothers reported children's symptoms of ADHD, symptoms of depression, and academic problems by questionnaire when the children were 8 years old., Results: Children of lowly educated parents scored higher on all outcomes and had an approximate doubling of the risk of high symptom levels. The association between maternal and paternal educational attainment and child symptoms of ADHD and academic problems persisted after controlling for shared genetic and family environmental factors. Phenotypic transmission to depression was weaker and in the best fitting model fully explained by genetic factors shared by the two generations., Conclusions: Associations between educational attainment of mothers and fathers and child symptoms of ADHD and academic problems could not be ascribed to shared familial risk factors, whereas associations with symptoms of depression could. Parental education or resources and behaviors resulting from low education might be targets of interventions aimed at reducing symptoms of ADHD and academic problems., (© 2020 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: A link between suboptimal fetal growth and higher risk of cardiovascular disease (CVD) is well documented. It has been difficult to assess the contribution of environmental versus genetic factors to the association, as these factors are closely connected in nuclear families. We investigated the association between offspring birthweight and CVD mortality in parents, aunts and uncles, and examined whether these associations are explained by CVD risk factors., Methods: We linked Norwegian data from the Medical Birth Registry, the Cause of Death Registry and cardiovascular surveys. A total of 1 353 956 births (1967-2012) were linked to parents and one maternal and one paternal aunt/uncle. Offspring birthweight and CVD mortality association among all relationships was assessed by hazard ratios (HR) from Cox regressions. The influence of CVD risk factors on the associations was examined in a subgroup., Results: Offspring birthweight was inversely associated with CVD mortality among parents and aunts/uncles. HR of CVD mortality for one standard deviation (SD) increase in offspring birthweight was 0.72 (0.69-0.75) in mothers and 0.89 (0.86-0.92) in fathers. In aunts/uncles, the HRs were between 0.90 (0.86-0.95) and 0.93 (0.91-0.95). Adjustment for CVD risk factors in a subgroup attenuated all the associations., Conclusions: Birthweight was associated with increased risk of CVD in parents and in aunts/uncles. These associations were largely explained by CVD risk factors. Our findings suggest that associations between offspring birthweight and CVD in adult relatives involve both behavioural variables (especially smoking) and shared genetics relating to established CVD risk factors., (© The Author(s) 2019. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Although microcephaly is a feature of Fetal Alcohol Syndrome, it is currently unknown whether low-to-moderate prenatal alcohol exposure affects head circumference. Small magnitude associations reported in observational studies are likely to be misleading due to confounding and misclassification biases. Alternative analytical approaches such as the use of family negative controls (e.g. comparing the effects of maternal and paternal exposure) could help disentangle causal effects. We investigated the association of maternal and paternal alcohol drinking before and early in pregnancy with infant head circumference, using data from 68,244 mother-father-offspring trios from the Norwegian Mother and Child Cohort Study (MoBa) (1999-2009). In analyses adjusted for potential confounders, we found no consistent pattern of association between maternal or paternal alcohol intake before or during pregnancy and offspring head circumference modelled as a continuous outcome. However, we found higher odds of microcephaly at birth for higher paternal, but not maternal, alcohol consumption before pregnancy, and similar but weaker effect estimates for first trimester drinking. Associations with paternal drinking before pregnancy were unexpected and should be regarded as hypothesis generating, until independently replicated, although potentially important given the absence of guidelines on safe drinking levels for men in couples trying for a pregnancy.

This is an update of the Norwegian Mother and Child Cohort Study (MoBa) cohort profile which was published in 2006. Pregnant women attending a routine ultrasound examination were initially invited. The first child was born in October 1999 and the last in July 2009. The participation rate was 41%. The cohort includes more than 114 000 children, 95 000 mothers and 75 000 fathers. About 1900 pairs of twins have been born. There are approximately 16 400 women who participate with more than one pregnancy. Blood samples were obtained from both parents during pregnancy and from mothers and children (umbilical cord) after birth. Samples of DNA, RNA, whole blood, plasma and urine are stored in a biobank. During pregnancy, the mother responded to three questionnaires and the father to one. After birth, questionnaires were sent out when the child was 6 months, 18 months and 3 years old. Several sub-projects have selected participants for in-depth clinical assessment and exposure measures. The purpose of this update is to explain and describe new additions to the data collection, including questionnaires at 5, 7, 8 and 13 years as well as linkages to health registries, and to point to some findings and new areas of research. Further information can be found at [www.fhi.no/moba-en]. Researchers interested in collaboration and access to the data can complete an electronic application available on the MoBa website above., (© The Author 2016; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Importance: Gastrointestinal (GI) comorbidities are frequently described in association with autism spectrum disorder (ASD). However, the prevalence of GI disturbances and the age at which such problems first appear are unclear, and their specificity for ASD compared with other neurodevelopmental disorders is uncertain., Objective: To compare maternal report of GI symptoms during the first 3 years of life in children with ASD, developmental delay (DD), and typical development (TD)., Design, Setting, and Participants: This large prospective cohort study consists of participants in the Norwegian Mother and Child Cohort Study. During a 10-year period (January 1, 1999, through December 31, 2008), women throughout Norway were recruited at the first prenatal ultrasonographic visit (approximately 18 weeks' gestation). The study enrolled 95,278 mothers, 75,248 fathers, and 114,516 children. Our analyses are based on MoBa data released through October 1, 2013, and NPR diagnoses registered through December 31, 2012, and include children born from January 1, 2002, through December 31, 2008, with completed age 18- and 36-month questionnaires., Exposures: We defined 3 groups of children: children with ASD (n = 195), children with DD and delayed language and/or motor development (n = 4636), and children with TD (n = 40 ,95)., Main Outcomes and Measures: The GI symptoms were based on maternal report of constipation, diarrhea, and food allergy/intolerance., Results: Children with ASD were at significantly increased odds of maternally reported constipation (adjusted odds ratio [aOR], 2.7; 95% CI, 1.9-3.8; P < .001) and food allergy/intolerance (aOR, 1.7; 95% CI, 1.1-2.6; P = .01) in the 6- to 18-month-old age period and diarrhea (aOR, 2.3; 95% CI, 1.5-3.6; P < .001), constipation (aOR, 1.6; 95% CI, 1.2-2.3; P < .01), and food allergy/intolerance (aOR, 2.0; 95% CI, 1.3-3.1; P < .01) in the 18- to 36-month-old age period compared with children with TD. Similar results for these symptom categories were observed in comparisons with children with DD, but ORs were slightly lower. Mothers of children with ASD were significantly more likely to report 1 or more GI symptom in either the 6- to 18-month or the 18- to 36-month-old age period and more than twice as likely to report at least 1 GI symptom in both age periods compared with mothers of children with TD or DD., Conclusions and Relevance: In this large prospective cohort, maternally reported GI symptoms are more common and more often persistent during the first 3 years of life in children with ASD than in children with TD or DD.

Objectives: The objective of the study was to investigate the associations among maternal prepregnancy BMI, paternal BMI, and the risk of autism spectrum disorders (ASDs) in children., Methods: The study sample of 92 909 children was derived from the population-based, prospective Norwegian Mother and Child Cohort Study. The age range was 4.0 through 13.1 (mean 7.4) years. Relative risks of ASDs were estimated by odds ratios (ORs) and 95% confidence intervals (CIs) from logistic regression models., Results: At the end of follow-up on December 31, 2012, 419 children in the study sample had been diagnosed with ASDs: 162 with autistic disorder, 103 with Asperger disorder, and 154 with pervasive developmental disorder not otherwise specified. Maternal obesity (BMI ≥30) was only weakly associated with ASD risk, whereas paternal obesity was associated with an increased risk of autistic disorder and Asperger disorder. The risk of autistic disorder was 0.27% (25 of 9267) in children of obese fathers and 0.14% (59 of 41 603) in children of fathers with normal weight (BMI <25), generating an adjusted OR of 1.73 (95% CI: 1.07-2.82). For Asperger disorder, analyses were limited to children aged ≥7 years (n = 50 116). The risk was 0.38% (18 of 4761) in children of obese fathers and 0.18% (42 of 22 736) in children of normal-weight fathers, and the adjusted OR was 2.01 (95% CI: 1.13-3.57). No associations were found for pervasive developmental disorder not otherwise specified., Conclusions: Paternal obesity is an independent risk factor for ASDs in children. The associations should be investigated further in genetic and epigenetic studies., (Copyright © 2014 by the American Academy of Pediatrics.)

Objective: To investigate course and predictors of eating disorders in the postpartum period., Method: A total of 77,807 women, participating in the Norwegian Mother and Child Cohort Study (MoBa), completed questionnaires during pregnancy including items covering DSM-IV criteria for prepregnancy anorexia nervosa (AN), bulimia nervosa (BN), eating disorder not otherwise specified (EDNOS-P), and binge eating disorder (BED). Additional questionnaires were completed at 18 and 36 months postpartum., Results: Proportions of women remitting at 18 months and 36 months postpartum were 50% and 59% for AN, 39% and 30% for BN, 46% and 57% for EDNOS-P, and 45% and 42% for BED, respectively. However, disordered eating persisted in a substantial proportion of women meeting criteria for either full or subthreshold eating disorders. BN during pregnancy increased the risk for continuation of BN. BMI and psychological distress were significantly associated with course of BED., Discussion: This is the first large-scale population-based study on course of eating disorders in the postpartum period. The results indicated that disordered eating persists in a substantial proportion of women with prepregnancy eating disorders. Health care professionals working with women in this phase of life need to pay specific attention to eating disorder symptoms and behaviors., (Copyright © 2013 Wiley Periodicals, Inc.)

Objective: We hypothesized that women with eating disorders would be more likely to rate their infants' temperament higher on negative emotionality than women without eating disorders., Method: Of 3,013 mothers with eating disorders, 44 reported anorexia nervosa (AN), 436 bulimia nervosa (BN), 2,475 binge eating disorder (BED), and 58 EDNOS purging type (EDNOS-P). The referent group comprised 45,964 mothers with no eating disorder. A partial proportional odds model was used to estimate the relation among maternal eating disorder presentations and infant temperament ratings while adjusting for covariates., Results: Women with AN, BN, EDNOS-P, and BED were 2.3, 1.4, 2.8, and 1.4 times more likely to report extreme fussiness than the referent group of women with no eating disorder, respectively., Discussion: Mothers with eating disorders may rate their infants as more difficult because of information-processing biases or because their infants are emotionally difficult. Maternal perception of infant temperament may be a risk factor for children's emotional development., (Copyright © 2011 Wiley Periodicals, Inc.)

Background: We have examined the association between socioeconomic status and risk of infant death in Norway between 1967 and 1998., Methods: Information from the Medical Birth Registry of Norway on all live births and infant deaths was linked to information from Statistics Norway on parents' education. There were 1,777,364 eligible live births and 15,517 infant deaths. Differences between educational-attainment groups were estimated as risk difference, relative risk, population-attributable fraction, and index of inequality ratio., Results: The risk of infant death decreased in all educational-attainment groups and the level of education increased over time. For neonatal (0-27 days of life) death the risk difference between infants whose mothers had high or low education was reduced from 3.5/1000 in the 1970s to 0.9/1000 in the 1990s. The inequality ratio declined from 1.72 to 1.32 and the population-attributable fraction from 22.3 to 8.4. For risk of postneonatal (28-364 days of life) death, the difference between infants whose mothers were in high or low education brackets increased from 0.7/1000 in the 1970s to 2.0/1000 in the 1990s. The inequality ratio went up from 1.31 to 4.00 and the population-attributable fraction from 9.7 to 39.5., Interpretation: Since the late 1960s, infant mortality has decreased and parental educational levels have risen. There is a higher degree of social equality with regard to risk of neonatal death, while the opposite holds for postneonatal death.