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Assortative mating on heritable traits can have implications for the genetic resemblance between siblings and in-laws in succeeding generations. We studied polygenic scores and phenotypic data from pairs of partners ( n  = 26,681), siblings ( n  = 2,170), siblings-in-law ( n  = 3,905), and co-siblings-in-law ( n  = 1,763) in the Norwegian Mother, Father and Child Cohort Study. Using structural equation models, we estimated associations between measurement error-free latent genetic and phenotypic variables. We found evidence of genetic similarity between partners for educational attainment ( r g  = 0.37), height ( r g  = 0.13), and depression ( r g  = 0.08). Common genetic variants associated with educational attainment correlated between siblings above 0.50 (r g  = 0.68) and between siblings-in-law ( r g  = 0.25) and co-siblings-in-law ( r g  = 0.09). Indirect assortment on secondary traits accounted for partner similarity in education and depression, but not in height. Comparisons between the genetic similarities of partners and siblings indicated that genetic variances were in intergenerational equilibrium. This study shows genetic similarities between extended family members and that assortative mating has taken place for several generations. Assortative mating could violate the assumption of random mating used in many genetic studies. Here, the authors study more than 25,000 Norwegian families to find genetic similarity between partners, siblings, and in-laws in genetic factors related to educational attainment, height, and depression.

Do associations between maternal anxiety symptoms and offspring mental health remain after comparing differentially exposed siblings? Participants were 17,724 offspring siblings and 11,553 mothers from the Norwegian Mother and Child Cohort study. Mothers reported anxiety and depressive symptoms at 30 weeks' gestation, and 0.5, 1.5, 3, and 5 years postpartum. Child internalizing and externalizing problems were assessed at ages 1.5, 3, and 5, and modeled using multilevel analyses with repeated measures nested within siblings, nested within mothers. Maternal pre- and postnatal anxiety were no longer associated with child internalizing or externalizing problems after adjusting for maternal depression and familial confounding. Maternal anxiety when the children were in preschool age, however, remained significantly associated with child internalizing but not externalizing problems.

Some studies show that children with obesity are more likely to receive a diagnosis of depression, anxiety, or attention-deficit hyperactivity disorder (ADHD). But this does not necessarily mean obesity causes these conditions. Depression, anxiety, or ADHD could cause obesity. A child's environment, including family income or their parents' mental health, could also affect a child's weight and mental health. Understanding the nature of these relationships could help scientists develop better interventions for both obesity and mental health conditions. Genetic studies may help scientists better understand the role of the environment in these conditions, but it's important to consider both the child's and their parents’ genetics in these analyses. This is because parents and children share not only genes, but also environmental conditions. For example, families that carry genetic variants associated with higher body weight might also have lower incomes, if parents have been affected by biases against heavier people in society and the workplace. Children in these families could have worse mental health because of effects of their parent’s weight, rather than their own weight. Looking at both child and adult genetics can help disentangle these processes. Hughes et al. show that a child's own body mass index, a ratio of weight and height, is not strongly associated with the child’s mental health symptoms. They analysed genetic, weight, and health survey data from about 41,000 8-year-old children and their parents. The results suggest that a child's own BMI does not have a large effect on their anxiety symptoms. There was also no clear evidence that a child's BMI affected their symptoms of depression or ADHD. These results contradict previous studies, which did not account for parental genetics. Hughes et al. suggest that, at least for eight-year-olds, factors linked with adult weight and which differ between families may be more critical to a child's mental health than a child’s own weight. For older children and adolescents, this may not be the case, and the individual’s own weight may be more important. As a result, policies designed to reduce obesity in mid-childhood are unlikely to greatly improve the mental health of children. On the other hand, policies targeting the environmental or societal factors contributing to higher body weights, bias against people with higher weights, and poor child mental health directly may be more beneficial.

Background Mental disorders often have onset early in life, contribute substantially to the global disease burden, and may interfere with young people’s ability to complete age-relevant tasks in important developmental periods. However, knowledge about prevalence and course of mental disorders in young adulthood is sparse. The aim of the current study was to estimate prevalence and stability of mental disorders from the twenties to the thirties/forties. Methods DSM-IV mental disorders were assessed with the Composite International Diagnostic Interview in two waves (1999–2004 and 2010–2011) in 1623 young adult Norwegian twins (63.2% women, aged 19–29 years in wave 1). Results In wave 1, the 12-month prevalence of any mental disorder among people in the twenties was 19.8% (men) and 32.4% (women), anxiety disorders: 9.6% (men) and 26.7% (women), anxiety disorders excluding specific phobias: 2.5% (men) and 6.9% (women), major depressive disorder (MDD): 4.4% (men) and 7.2% (women), and alcohol use disorder (AUD): 8.7% (men) and 4.4% (women). The prevalence of any mental disorder decreased from the twenties to the thirties/forties. This was due to a decrease in AUD and specific phobias. Anxiety disorders in the twenties predicted anxiety disorders and MDD ten years later, even when controlling for the association between these disorders in the twenties. MDD in the twenties predicted MDD ten years later. At both ages, two-week and 12-month prevalence estimates differed markedly for MDD - indicating an episodic course. Conclusions Common mental disorders are highly prevalent among young adults in the twenties, and somewhat less prevalent in the thirties/forties. Those who suffer from one mental disorder in the twenties are at considerably increased risk for suffering from a disorder ten years later as well. This may have significant implications for young people’s ability to attain education, establish a family, and participate in occupational life.

Background Maternal acetaminophen use during pregnancy is associated with increased risk of ADHD in the child. This could reflect causal influence of acetaminophen on fetal neurodevelopment or could be due to confounding factors. The aim of the current study was to examine unmeasured familial confounding factors of this association. Methods We used data from 26,613 children from 12,902 families participating in the prospective Norwegian Mother, Father, and Child Cohort Study (MoBa). The MoBa was linked to the Norwegian Medical Birth Register and the Norwegian Patient Registry. Siblings discordant for prenatal acetaminophen exposure were compared regarding risk of having an ADHD diagnosis. Results Children exposed to acetaminophen up to 28 days during pregnancy did not have increased risk of receiving an ADHD diagnosis compared to unexposed children. The adjusted Hazard ratio (aHR) was 0.87 (95% C.I. = 0.70‐1.08) for exposure 1 to 7 days, and 1.13 (95% C.I. = 0.82–1.49) for 8–28 days. Long‐term exposure (29 days or more) was associated with a two‐fold increase in risk of ADHD diagnosis (aHR = 2.02, 95% C.I = 1.17–3.25). In the sibling control model, the association between long‐term acetaminophen use and ADHD in the child was aHR = 2.77 (95% C.I. = 1.48–5.05) at the between‐family level, and aHR = 1.06 (95% C.I. = 0.51–2.05) at the within‐family level. Conclusions Both the exposed and the unexposed children of mothers with long‐term use of acetaminophen in one of the pregnancies had increased risk of receiving an ADHD diagnosis. This indicates that the observed association between long‐term acetaminophen use during pregnancy and ADHD in the child may at least partly be confounded by unobserved family factors.

Twin data permit decomposition of comorbidity into genetically and environmentally derived correlations. No previous twin study includes all major forms of anxiety disorder. To estimate the degree to which genetic and environmental risk factors are shared rather than unique to dimensionally scored panic disorder, generalised anxiety disorder, phobias, obsessive-compulsive disorder and post-traumatic stress disorder. Data obtained from 2801 young-adult Norwegian twins by means of the Composite International Diagnostic Interview were analysed with the Mx program. A multivariate common factor model fitted best. The latent liability to all anxiety disorders was substantially more heritable (54%) than the individual disorders (23% to 40%). Most of the genetic effect was common to the disorders. Genes contributed just over 50% to the covariance between liabilities. The five anxiety disorders all share genetic and environmental risk factors. This has implications for the revision of the anxiety disorder section in DSM-V.

Triclosan (TCS) is a synthetic antibacterial chemical that is used in personal care products and is measurable in urine. Urinary TCS has been associated with allergy in children in Norway and the United States. A reasonable degree of temporal reliability of TCS urinary concentrations has been reported among US children as well as for Puerto Rican pregnant women. We examined the reliability of TCS measures in urine among Norwegian pregnant women. TCS was measured in spot urine samples collected in gestational weeks 17, 23, and 29 from 45 women in The Norwegian Mother and Child Cohort Study (MoBa) enrolled in 2007 and 2008. Spearman’s rank correlation coefficient ( r s ) and intraclass correlation coefficient (ICC) statistics were calculated. Fifty-six percent of the 45 women had a least one sample with a value above the method limit of detection (2.3 μg/l). The correlation coefficients were 0.61 for TCS concentrations at 17 and 23 weeks and 0.49 for concentrations at 17 and 29 weeks. For the three time points, the ICC was 0.49. The reliability of TCS concentrations in repeated urine samples from pregnant Norwegian women was reasonably good, suggesting a single urine sample can adequately represent TCS exposure during pregnancy.

Background Maternal infections during pregnancy are common events that have been suggested to be risk factors for Attention‐deficit hyperactivity disorder (ADHD) in offspring. Only a few studies have been conducted to date and results are conflicting. The current study investigates the associations between specific groups of prenatal maternal infections and offspring ADHD, considering timing of exposure and the role of fever. Methods We used data from the prospective Norwegian Mother, Father and Child Cohort Study (MoBa), including more than 112,000 pregnancies, linked with data from the Medical Birth Registry of Norway and the Norwegian Patient Registry to estimate odds ratios for the likelihood that children develop ADHD after being exposed to maternal infections during gestation. Results Children exposed to any maternal infection during pregnancy showed increased risk of receiving an ADHD diagnosis (OR = 1.15, CI = 1.03–1.27). Specifically, increased ADHD risk was observed after exposure to genitourinary infections in second (OR = 1.42, CI = 1.06–1.90) or third trimester (OR = 2.04, CI = 1.19–3.49), and to respiratory infections in second trimester (OR = 1.31, CI = 1.12–1.54), provided these infections were accompanied by episodes of fever. Increased ADHD risk was also observed after exposure to diarrhea without fever in the third trimester (OR = 1.25, CI = 1.07–1.46). Conclusions Overall, our results suggest that prenatal exposure to maternal infections, particularly with co‐occurring episodes of fever, are risk factors for ADHD. Fever (or severity of the infection) appears to be more important in mid‐pregnancy associations. Our results indicate that type of infection and timing of exposure might influence the associations, but small effect sizes require careful interpretations. The association between infection and ADHD should be estimated using discordant siblings or other negative control designs that give better adjustment for unmeasured familial confounding. The current study investigates the associations between specific groups of prenatal maternal infections and offspring ADHD, taking into account timing of exposure and the role of fever. Results suggest that prenatal exposure to maternal infections, particularly with co‐occurring episodes of fever, are risk factors for ADHD but that type of infection and timing of exposure are important factors. Fever (or severity of the infection) appears to be more important in mid‐pregnancy associations. In late pregnancy diarrhea without co‐occurring fever was associated with increased risk of ADHD, suggesting there may be other aspects of such infections that contribute to pathogenesis nearer to term.

Background Children of parents with high levels of neuroticism tend to have high neuroticism themselves as well as increased risk of experiencing symptoms of anxiety and depression. It is not yet clear how much of this link is attributable to a potential effect of parent on child (e.g., via a socializing effect) versus to shared genetic risk. We aimed to determine whether there is an intergenerational association after accounting for genetic transmission and assortative mating. Methods We used data from the Norwegian Mother, Father and Child Cohort Study including 11,088 sibling pairs in the parental generation, their partners (N = 22,176) and their offspring (N = 26,091). Exposures were maternal and paternal neuroticism (self‐reported), and the outcomes were neuroticism, symptoms of depression, and symptoms of anxiety in 8‐year‐old children (mother‐reported). Results After accounting for assortative mating in parents (phenotypic r = 0.26) and genetic transmission (explaining 0%–18% of the mother‐offspring correlations), potential maternal effects explained 80% (95% CI = 47–95) of the association with offspring neuroticism (mother‐child r = 0.31), 78% (95% CI = 66–89) of the association with offspring depressive symptoms (r = 0.31), and 98% (95% CI = 45–112) of the association with offspring anxiety symptoms (r = 0.16). Intergenerational transmission of genetic variants associated with paternal neuroticism accounted for ∼40% (CI = 22%–58%) of the father‐offspring correlations with neuroticism and symptoms of depression (r = 0.13 and 0.13, respectively) but none with offspring symptoms of anxiety (r = 0.05). The remaining father‐offspring correlations were explained by maternal influences through assortative mating. Conclusions These results are consistent with direct effects between maternal and offspring neuroticism and between maternal neuroticism and offspring symptoms of anxiety and depression. Further understanding of these intergenerational processes will require an adequate model of how these constructs (neuroticism, anxiety and depression) relate to each other within generations.

There is growing concern that phthalate exposures may have an impact on child neurodevelopment. Prenatal exposure to phthalates has been linked with externalizing behaviors and executive functioning defects suggestive of an attention-deficit hyperactivity disorder (ADHD) phenotype. We undertook an investigation into whether prenatal exposure to phthalates was associated with clinically confirmed ADHD in a population-based nested case-control study of the Norwegian Mother and Child Cohort (MoBa) between the years 2003 and 2008. Phthalate metabolites were measured in maternal urine collected at midpregnancy. Cases of ADHD ( =297) were obtained through linkage between MoBa and the Norwegian National Patient Registry. A random sample of controls ( =553) from the MoBa population was obtained. In multivariable adjusted coexposure models, the sum of di-2-ethylhexyl phthalate metabolites (∑DEHP) was associated with a monotonically increasing risk of ADHD. Children of mothers in the highest quintile of ∑DEHP had almost three times the odds of an ADHD diagnosis as those in the lowest [OR=2.99 (95% CI: 1.47, 5.49)]. When ∑DEHP was modeled as a log-linear (natural log) term, for each log-unit increase in exposure, the odds of ADHD increased by 47% [OR=1.47 (95% CI: 1.09, 1.94)]. We detected no significant modification by sex or mediation by prenatal maternal thyroid function or by preterm delivery. In this population-based case-control study of clinical ADHD, maternal urinary concentrations of DEHP were monotonically associated with increased risk of ADHD. Additional research is needed to evaluate potential mechanisms linking phthalates to ADHD. https://doi.org/10.1289/EHP2358.