The observed association between maternal anxiety and adolescent asthma : children of twin design suggest familial effects

BACKGROUND: Previous studies indicate that maternal anxiety is associated with asthma in the adolescent child, but mechanisms are unclear. OBJECTIVE: To investigate the association between maternal anxiety and maternal, self- and register-based report of asthma in the adolescent child, and whether the association remains after control of familial confounding (shared environmental and genetic factors). METHOD: From the Twin and Offspring Study of Sweden, 1691 mothers (1058 twins) and their adolescent child were included. The association between maternal self-reported anxiety (Beck Anxiety Inventory (BAI) and Karolinska Scales of Personality (KSP) somatic or psychic anxiety) and asthma based on subjective (maternal or child report) or objective (register-based diagnosis and medication) measures were analysed using logistic regression. The children-of-twins design was used to explore whether genes or environment contribute to the association. RESULTS: Maternal BAI anxiety (OR 2.02, CI 1.15-3.55) was significantly associated with adolescent asthma reported by the mother. Maternal KSP somatic anxiety (OR 1.74, CI 1.04-2.91) and psychic anxiety (OR 1.74, CI 1.05-2.86) was significantly associated with breathlessness reported by the adolescent child. In contrast, maternal anxiety was not associated with increased risk for the register-based outcomes of asthma diagnosis or medication. The results remained also after adjusting for covariates and the children-of-twins analyses which indicate that the association was due to familial confounding. CONCLUSIONS: We found some associations between maternal anxiety and subjectively reported offspring asthma or breathlessness which may be due to familial effects. A likely candidate for explaining this familial confounding is heritable personality traits associated with both anxiety and subjective measures of asthma.NonePublishe

Longitudinal examination of pathways to peer problems in middle childhood: a siblings-reared-apart design

To advance research from Dishion and others on associations between parenting and peer problems across childhood, we used a sample of 173 sibling pairs reared apart since birth (because of adoption of one of the siblings) to examine associations between parental hostility and children’s peer problems when children were ages 7 and 9.5 years (n = 326 children). We extended conventional cross-lagged parent–peer models by incorporating child inhibitory control as an additional predictor and examining genetic contributions via birth mother psychopathology. Path models indicated a cross-lagged association from parental hostility to later peer problems. When child inhibitory control was included, birth mother internalizing symptoms were associated with poorer child inhibitory control, which was associated with more parental hostility and peer problems. The cross-lagged paths from parental hostility to peer problems were no longer significant in the full model. Multigroup analyses revealed that the path from birth mother internalizing symptoms to child inhibitory control was significantly higher for birth parent–reared children, indicating the possible contribution of passive gene–environment correlation to this association. Exploratory analyses suggested that each child’s unique rearing context contributed to their inhibitory control and peer behavior. Implications for the development of evidence-based interventions are discussed

Toward an Understanding of the Role of the Environment in the Development of Early Callous Behavior

Key to understanding the long‐term impact of social inequalities is identifying early behaviors that may signal higher risk for later poor psychosocial outcomes, such as psychopathology. A set of early‐emerging characteristics that may signal risk for later externalizing psychopathology is callous‐unemotional (CU) behavior. CU behavior predicts severe and chronic trajectories of externalizing behaviors in youth. However, much research on CU behavior has focused on late childhood and adolescence, with little attention paid to early childhood when preventative interventions may be most effective. In this article, we summarize our recent work showing that (a) CU behavior can be identified in early childhood using items from common behavior checklists, (b) CU behavior predicts worse outcomes across early childhood, (c) CU behavior exhibits a nomological network distinct from other early externalizing behaviors, and (d) malleable environmental factors, particularly parenting, may play a role in the development of early CU behaviors. We discuss the challenges of studying contextual contributors to the development of CU behavior in terms of gene–environment correlations and present initial results from work examining CU behavior in an adoption study in which gene–environment correlations are examined in early childhood. We find that parenting is a predictor of early CU behavior even in a sample in which parents are not genetically related to the children.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/136006/1/jopy12221_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/136006/2/jopy12221.pd

Disentangling genetic and environmental influences on early language development: The interplay of genetic propensity for negative emotionality and surgency, and parenting behavior effects on early language skills in an adoption study

Parenting and children's temperament are important influences on language development. However, temperament may reflect prior parenting, and parenting effects may reflect genes common to parents and children. In 561 U.S. adoptees (57% male) and their birth and rearing parents (70% and 92% White, 13% and 4% African American, and 7% and 2% Latinx, respectively), this study demonstrated how genetic propensity for temperament affects language development, and how this relates to parenting. Genetic propensity for negative emotionality inversely predicted language at 27 months (β = −.15) and evoked greater maternal warmth (β = .12), whereas propensity for surgency positively predicted language at 4.5 years (β = .20), especially when warmth was low. Parental warmth (β = .15) and sensitivity (β = .19) further contributed to language development, controlling for common gene effects

Additive drug-specific and sex-specific risks associated with co-use of marijuana and tobacco during pregnancy: Evidence from 3 recent developmental cohorts (2003-2015).

BACKGROUND: Methodologic challenges related to the concomitant use (co-use) of substances and changes in policy and potency of marijuana contribute to ongoing uncertainty about risks to fetal neurodevelopment associated with prenatal marijuana use. In this study, we examined two biomarkers of fetal neurodevelopmental risk-birth weight and length of gestation-associated with prenatal marijuana use, independent of tobacco (TOB), alcohol (ALC), other drug use (OTH), and socioeconomic risk (SES), in a pooled sample (N = 1191) derived from 3 recent developmental cohorts (2003-2015) with state-of-the-art substance use measures. We examined differential associations by infant sex, and multiplicative effects associated with co-use of MJ and TOB. METHODS: Participants were mother-infant dyads with complete data on all study variables derived from Growing Up Healthy (n = 251), Behavior and Mood in Babies and Mothers (Cohorts 1 and 2; n = 315), and the Early Growth and Development Study (N = 625). We estimated direct effects on birth weight and length of gestation associated with MJ, TOB, and co-use (MJ x TOB), using linear regression analysis in the full sample, and in male (n = 654) and female (n = 537) infants, separately. RESULTS: Mean birth weight and length of gestation were 3277 g (SD = 543) and 37.8 weeks (SD = 2.0), respectively. Rates of prenatal use were as follows: any use, n = 748 (62.8%); MJ use, n = 273 (22.9%); TOB use, n = 608 (51.0%); co-use of MJ and TOB, n = 230 (19.3%); ALC use, n = 464 (39.0%); and OTH use n = 115 (9.7%.) For all infants, unique effects on birth weight were observed for any MJ use [B(SE) = -84.367(38.271), 95% C.I. -159.453 to -9.281, p = .028], any TOB use [B(SE) = -0.99.416(34.418), 95% C.I. -166.942 to -31.889, p = .004], and each cigarette/day in mean TOB use [B(SE) = -12.233(3.427), 95% C.I. -18.995 to -5.510, p \u3c .001]. Additional effects of co-use on birth weight, beyond these drug-specific effects, were not supported. In analyses stratified by sex, while TOB use was associated with lower birth weight in both sexes, MJ use during pregnancy was associated with lower birth weight of male infants [B(SE) = -153.1 (54.20); 95% C.I. -259.5 to -46.7, p = .005], but not female infants [B(SE) = 8.3(53.1), 95% C.I. -96.024 to 112.551, p = .876]. TOB, MJ, and their co-use were not associated with length of gestation. CONCLUSIONS: In this sample, intrauterine co-exposure to MJ and TOB was associated with an estimated 18% reduction in birth weight not attributable to earlier delivery, exposure to ALC or OTH drugs, nor to maternal SES. We found evidence for greater susceptibility of male fetuses to any prenatal MJ exposure. Examination of dose-dependence in relationships found in this study, using continuous measures of exposure, is an important next step. Finally, we underscore the need to consider (a) the potential moderating influence of fetal sex on exposure-related neurodevelopmental risks; and (b) the importance of quantifying expressions of risk through subtle alterations, rather than dichotomous outcomes

Family interactions in toddlerhood influence social competence in preschool age: Accounting for genetic and prenatal influences

Identification of early promotive and risk factors for social competence is important for fostering children’s successful social development; particularly given social competence is essential for children’s later academic and psychological well-being. While research suggests that the early parent–child relationship, genetics, and prenatal influences are associated with social competence, there is less research considering how these factors may operate together to shape children’s social competence in early childhood. Using a genetically informed sample from the Early Growth and Development Study (N = 561), we examined multiple levels of influence (i.e., genetic, prenatal, parenting, and child characteristics) on children’s social competence at 4.5 years old. Results from structural equation models showed adoptive mother overreactivity at 18 months was positively associated with child dysregulation at 27 months, which, in turn, was associated with lower levels of social competence at 4.5 years. Also, child reactivity at 18 months was independently associated with higher levels of adoptive mother overreactivity at 27 months, which, in turn, was associated with lower levels of social competence at 4.5 years. Finally, we found an evocative effect on adoptive fathers’ overreactivity at 18 months such that prenatal birth mother distress was negatively associated with adoptive fathers’ overreactivity at 18 months. Overall, this study found evidence for genetic influences, and bidirectional associations between parent and child in toddlerhood that are related to lower levels of social competence when children were 4.5 years old. We also found that the prenatal environment was associated with parenting, but not with child behavior directly. This study’s ability to simultaneously examine multiple domains of influence helps provide a more comprehensive picture of important mechanisms and developmental periods for children’s early social competence

Using an adoption–biological family design to examine associations between maternal trauma, maternal depressive symptoms, and child internalizing and externalizing behaviors

Maternal trauma is a complex risk factor that has been linked to adverse child outcomes, yet the mechanisms underlying this association are not well understood. This study, which included adoptive and biological families, examined the heritable and environmental mechanisms by which maternal trauma and associated depressive symptoms are linked to child internalizing and externalizing behaviors. Path analyses were used to analyze data from 541 adoptive mother–adopted child (AM–AC) dyads and 126 biological mother–biological child (BM–BC) dyads; the two family types were linked through the same biological mother. Rearing mother’s trauma was associated with child internalizing and externalizing behaviors in AM–AC and BM–BC dyads, and this association was mediated by rearing mothers’ depressive symptoms, with the exception of biological child externalizing behavior, for which biological mother trauma had a direct influence only. Significant associations between maternal trauma and child behavior in dyads that share only environment (i.e., AM–AC dyads) suggest an environmental mechanism of influence for maternal trauma. Significant associations were also observed between maternal depressive symptoms and child internalizing and externalizing behavior in dyads that were only genetically related, with no shared environment (i.e., BM–AC dyads), suggesting a heritable pathway of influence via maternal depressive symptoms