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The Early Growth and Development Study (EGDS) is a prospective adoption study of birth parents, adoptive parents and adopted children (n = 561 adoptees). The original sample has been expanded to include siblings of the EGDS adoptees who were reared by the birth mother and assessed beginning at age 7 years (n = 217 biological children), and additional siblings in both the birth and adoptive family homes, recruited when the adoptees were 8–15 years old (n = 823). The overall study aims are to examine how family, peer and contextual processes affect child and adolescent adjustment, and to examine their interplay (mediation, moderation) with genetic influences. Adoptive and birth parents were originally recruited through adoption agencies located throughout the USA following the birth of a child. Assessments are ongoing and occurred in 9 month’s intervals until the adoptees turned 3 years of age, and in 1 to 2 year intervals thereafter through age 15. Data collection includes the following primary constructs: child temperament, behavior problems, mental health, peer relations, executive functioning, school performance and health; birth and adoptive parent personality characteristics, mental health, health, context, substance use, parenting and marital relations; and the prenatal environment. Findings highlight the power of the adoption design to detect environmental influences on child development and provide evidence of complex interactions and correlations between genetic, prenatal environmental and postnatal environmental influences on a range of child outcomes. The study sample, procedures and an overview of findings are summarized and ongoing assessment activities are described.
To advance research from Dishion and others on associations between parenting and peer problems across childhood, we used a sample of 177 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 = 329 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 his or her inhibitory control and peer behavior. Implications for the development of evidence-based interventions are discussed.
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.
Associations between parenting and child outcomes are often interpreted as reflecting causal, social influences. However, such associations may be confounded by genes common to children and their biological parents. To the extent that these shared genes influence behaviours in both generations, a passive genetic mechanism may explain links between them. Here we aim to quantify the relative importance of passive genetic v. social mechanisms in the intergenerational association between parent–offspring relationship quality and offspring internalizing problems in adolescence.
We used a Children-of-Twins (CoT) design with data from the parent-based Twin and Offspring Study of Sweden (TOSS) sample [909 adult twin pairs and their offspring; offspring mean age 15.75 (2.42) years], and the child-based Swedish Twin Study of CHild and Adolescent Development (TCHAD) sample [1120 adolescent twin pairs; mean age 13.67 (0.47) years]. A composite of parent-report measures (closeness, conflict, disagreements, expressions of affection) indexed parent–offspring relationship quality in TOSS, and offspring self-reported internalizing symptoms were assessed using the Child Behavior Checklist (CBCL) in both samples.
A social transmission mechanism explained the intergenerational association [r = 0.21 (0.16–0.25)] in our best-fitting model. A passive genetic transmission pathway was not found to be significant, indicating that parental genetic influences on parent–offspring relationship quality and offspring genetic influences on their internalizing problems were non-overlapping.
These results indicate that this intergenerational association is a product of social interactions between children and parents, within which bidirectional effects are highly plausible. Results from genetically informative studies of parenting-related effects should be used to help refine early parenting interventions aimed at reducing risk for psychopathology.
Early callous–unemotional behaviours identify children at risk for
antisocial behaviour. Recent work suggests that the high heritability of
callous–unemotional behaviours is qualified by interactions with positive
To examine whether heritable temperament dimensions of fearlessness and
low affiliative behaviour are associated with early callous–unemotional
behaviours and whether parenting moderates these associations.
Using an adoption sample (n=561), we examined pathways
from biological mother self-reported fearlessness and affiliative
behaviour to child callous–unemotional behaviours via observed child
fearlessness and affiliative behaviour, and whether adoptive parent
observed positive parenting moderated pathways.
Biological mother fearlessness predicted child callous–unemotional
behaviours via earlier child fearlessness. Biological mother low
affiliative behaviour predicted child callous–unemotional behaviours,
although not via child affiliative behaviours. Adoptive mother positive
parenting moderated the fearlessness to callous–unemotional behaviour
Heritable fearlessness and low interpersonal affiliation traits
contribute to the development of callous–unemotional behaviours. Positive
parenting can buffer these risky pathways.
Studies of the role of the early environment in shaping children’s risk for anxiety problems have produced mixed results. It is possible that inconsistencies in previous findings result from a lack of consideration of a putative role for inherited influences moderators on the impact of early experiences. Early inherited influences not only contribute to vulnerabilities for anxiety problems throughout the lifespan, but can also modulate the ways that the early environment impacts child outcomes. In the current study, we tested the effects of child-centered parenting behaviors on putative anxiety risk in young children who differed in levels of inherited vulnerability. We tested this using a parent–offspring adoption design and a sample in which risk for anxiety problems and parenting behaviors were assessed in both mothers and fathers. Inherited influences on anxiety problems were assessed as anxiety symptoms in biological parents. Child-centered parenting was observed in adoptive mothers and fathers when children were 9 months old. Social inhibition, an early temperament marker of anxiety risk, was observed at child ages 9 and 18 months. Inherited influences on anxiety problems moderated the link between paternal child-centered parenting during infancy and social inhibition in toddlerhood. For children whose birth parents reported high levels of anxiety symptoms, greater child-centered parenting in adoptive fathers was related to greater social inhibition 9 months later. For children whose birth parents reported low levels of anxiety symptoms, greater child-centered parenting in adoptive fathers was related to less social inhibition across the same period.
Real-time detection of microlensing has moved from proof of concept in 1994 (Udalski et al. 1994a, Alcock et al. 1994) to a steady stream of events this year. Global dissemination of these events by the MACHO and OGLE collaborations has made possible intensive photometric and spectroscopic follow up from widely dispersed sites confirming the microlensing hypothesis (Benetti 1995). Improved photometry and increased temporal resolution from follow up observations greatly increases the possibility of detecting deviations from the standard point-source, point-lens, inertial motion microlensing model. These deviations are crucial in understanding individual lensing systems by breaking the degeneracy between lens mass, position and velocity. We report here on GMAN (Global Microlensing Alert Network), the coordinated follow up of MACHO alerts.
Gravitational microlensing is the most straightforward interpretation of the stellar brightenings that have been observed by our team and other experiments. These data have provided some of the most stringent limits to date on the nature of the Galaxy's dark matter halo. The number of events seen towards the LMC indicate that our Galaxy is not surrounded by a “standard” halo of MACHOs in the mass range of 10–6 to 0.3 solar masses. The observed optical depth towards the Galactic Center is an important constraint on the distribution of mass in the plane of the Galaxy.
Parental depressive symptoms are associated with emotional and behavioural problems in offspring. However, genetically informative studies are needed to distinguish potential causal effects from genetic confounds, and longitudinal studies are required to distinguish parent-to-child effects from child-to-parent effects.
We conducted cross-sectional analyses on a sample of Swedish twins and their adolescent offspring (n = 876 twin families), and longitudinal analyses on a US sample of children adopted at birth, their adoptive parents, and their birth mothers (n = 361 adoptive families). Depressive symptoms were measured in parents, and externalizing and internalizing problems measured in offspring. Structural equation models were fitted to the data.
Results of model fitting suggest that associations between parental depressive symptoms and offspring internalizing and externalizing problems remain after accounting for genes shared between parent and child. Genetic transmission was not evident in the twin study but was evident in the adoption study. In the longitudinal adoption study child-to-parent effects were evident.
We interpret the results as demonstrating that associations between parental depressive symptoms and offspring emotional and behavioural problems are not solely attributable to shared genes, and that bidirectional effects may be present in intergenerational associations.
Risk factors for the childhood development of co-occurring internalizing and externalizing symptoms are not well understood, despite a high prevalence and poor clinical outcomes associated with this co-occurring phenotype. We examined inherited and environmental risk factors for co-occurring symptoms in a sample of children adopted at birth and their birth mothers and adoptive mothers (N = 293). Inherited risk factors (i.e., birth mothers' processing speed and internalizing symptoms) and environmental risk factors (i.e., adoptive mothers' processing speed, internalizing symptoms, and uninvolved parenting) were examined as predictors for the development of internalizing-only, externalizing-only, or co-occurring symptoms using structural equation modeling. Results suggested a unique pattern of predictive factors for the co-occurring phenotype, with risk conferred by adoptive mothers' uninvolved parenting, birth mothers' slower processing speed, and the birth mothers' slower processing speed in tandem with adoptive mothers' higher internalizing symptoms. Additional analyses indicated that when co-occurring-symptom children were incorporated into internalizing and externalizing symptom groups, differential risk factors for externalizing and internalizing symptoms emerged. The findings suggest that spurious results may be found when children with co-occurring symptoms are not examined as a unique phenotypic group.
Past research has documented pervasive genetic influences on emotional and behavioral disturbance across the life span and on liability to adult psychiatric disorder. Increasingly, interest is turning to mechanisms of gene–environment interplay in attempting to understand the earliest manifestations of genetic risk. We report findings from a prospective adoption study, which aimed to test the role of evocative gene–environment correlation in early development. Included in the study were 561 infants adopted at birth and studied between 9 and 27 months, along with their adoptive parents and birth mothers. Birth mother psychiatric diagnoses and symptoms scales were used as indicators of genetic influence, and multiple self-report measures were used to index adoptive mother parental negativity. We hypothesized that birth mother psychopathology would be associated with greater adoptive parent negativity and that such evocative effects would be amplified under conditions of high adoptive family adversity. The findings suggested that genetic factors associated with birth mother externalizing psychopathology may evoke negative reactions in adoptive mothers in the first year of life, but only when the adoptive family environment is characterized by marital problems. Maternal negativity mediated the effects of genetic risk on child adjustment at 27 months. The results underscore the importance of genetically influenced evocative processes in early development.
Attention control plays an important role in the development of internalizing symptoms in children. We explored the degree to which infants' genetic and environmentally based risk moderated the link between attention control and internalizing problems during toddlerhood. These associations were examined within a prospective adoption design, enabling the disentanglement of genetic and environmental risk for internalizing problems. Attention control in adopted infants was observed during periods of distress at age 9 months. Birth parents' anxiety symptoms were used as an index of genetic risk, while adoptive parents' anxiety symptoms were used as an index of environmental risk. Adoptive mothers and fathers reported on children's internalizing problems when children were 18 and 27 months old. Greater attention control in infancy appeared to mitigate genetically based risk for internalizing problems during toddlerhood when children were raised by adoptive parents who were low in anxiety. Findings suggest that for genetically susceptible children who are raised in low-risk environments, attention control may provide a protective factor against developing internalizing problems across early life.
To better understand mechanisms underlying the intergenerational transmission of social anxiety, we used a prospective adoption design to examine the roles of genetic influences (inferred from birth mothers' social phobia) and rearing environment (adoptive mothers' and fathers' responsiveness) on the development of socially inhibited, anxious behaviors in children between 18 and 27 months of age. The sample consisted of 275 adoption-linked families, each including an adopted child, adoptive parents, and a birth mother. Results indicated that children whose birth mothers met criteria for the diagnosis of social phobia showed elevated levels of observed behavioral inhibition in a social situation at 27 months of age if their adoptive mothers provided less emotionally and verbally responsive rearing environments at 18 months of age. Conversely, in the context of higher levels of maternal responsiveness, children of birth mothers with a history of social phobia did not show elevated levels of behavioral inhibition. These findings on maternal responsiveness were replicated in a model predicting parent reports of child social anxiety. The findings are discussed in terms of gene–environment interactions in the intergenerational transmission of social anxiety.
The Early Growth and Development Study is a prospective adoption study of birth parents, adoptive parents, and adopted children recruited in two cohorts (N = 561 triads). The primary study aims are to examine how family, peer, and contextual processes affect children's adjustment, and to examine their interplay (mediation, moderation) with genetic influences. Participants were recruited through adoption agencies located throughout the United States following the birth of a child. Assessments are ongoing, in 9-month intervals until the child reaches 3 years of age and in 1-year intervals thereafter through age 9. Data collection includes the following primary constructs: child temperament, social behavior, school performance, mental health, and health; birth and adoptive parent personality characteristics, mental health, competence, stress, health, context, substance use, parenting, and marital relations; and pregnancy use of drugs and maternal stress during pregnancy. DNA and salivary cortisol samples have also been collected. Analyses have indicated evidence for genotype-environment interactions during early childhood. Study procedures, sample representativeness (including tests of potential confounds in the adoption design), and an overview of findings to date are summarized, and future plans are described.
The current study examines the interplay between parental overreactivity and children's genetic backgrounds as inferred from birth parent characteristics on the development of negative emotionality during infancy, and in turn, to individual differences in externalizing problems in toddlerhood. The sample included 361 families linked through adoption (birth parents and adoptive families). Data were collected when the children were 9, 18, and 27 months old. Results indicated links between individual levels and changes in negative emotionality during infancy and toddlerhood to externalizing problems early in the third year of life. Findings also revealed an interaction between birth mother negative affect and adoptive mother overreactive parenting on children's negative emotionality. This Genotype × Environment interaction predicted externalizing problems indirectly through its association with negative emotionality and revealed stronger effects of genetic risk for children with less overreactive parenting from their mothers. Limitations of this study and directions for future research are discussed.
Anisotropic, noble metal nanoparticles have been synthesized using a template synthesis strategy. In short, metallic salts are reduced in the nanometer scale pores of either an alumina or polycarbonate membrane. The particles can then been released from the template to form suspensions of anisotropic nanoparticles. These nanoparticles have been modified with deoxyribonucleic acid (DNA) oligomers of varying length using several different attachment chemistries. The thermodynamics and kinetics of modifying these particles with DNA has been explored. DNA has also been used to assemble the particles on planar Au surfaces as well as lithographically defined Au pads on Si wafers. In addition to surface assembly, DNA has been used to assemble the nanowires into simple, yet deterministic structures in solution.