Disentangling nature from nurture in examining the interplay between parent-child relationships, ADHD, and early academic attainment.

BACKGROUND: Attention deficit hyperactivity disorder (ADHD) is highly heritable and is associated with lower educational attainment. ADHD is linked to family adversity, including hostile parenting. Questions remain regarding the role of genetic and environmental factors underlying processes through which ADHD symptoms develop and influence academic attainment. METHOD: This study employed a parent-offspring adoption design (N = 345) to examine the interplay between genetic susceptibility to child attention problems (birth mother ADHD symptoms) and adoptive parent (mother and father) hostility on child lower academic outcomes, via child ADHD symptoms. Questionnaires assessed birth mother ADHD symptoms, adoptive parent (mother and father) hostility to child, early child impulsivity/activation, and child ADHD symptoms. The Woodcock-Johnson test was used to examine child reading and math aptitude. RESULTS: Building on a previous study (Harold et al., 2013, Journal of Child Psychology and Psychiatry, 54(10), 1038-1046), heritable influences were found: birth mother ADHD symptoms predicted child impulsivity/activation. In turn, child impulsivity/activation (4.5 years) evoked maternal and paternal hostility, which was associated with children's ADHD continuity (6 years). Both maternal and paternal hostility (4.5 years) contributed to impairments in math but not reading (7 years), via impacts on ADHD symptoms (6 years). CONCLUSION: Findings highlight the importance of early child behavior dysregulation evoking parent hostility in both mothers and fathers, with maternal and paternal hostility contributing to the continuation of ADHD symptoms and lower levels of later math ability. Early interventions may be important for the promotion of child math skills in those with ADHD symptoms, especially where children have high levels of early behavior dysregulation.

Utilising Genetically-Informed Research Designs to Better Understand Family Processes and Child Development: Implications for Adoption and Foster Care Focused Interventions.

Understanding the interplay between genetic factors and family environmental processes (e.g., inter-parental relationship quality, positive versus negative parenting practices) and children's mental health (e.g., anxiety, depression, conduct problems, ADHD) in the contexts of adoption and foster-care research and practice is critical for effective prevention and intervention programme development. Whilst evidence highlights the importance of family environmental processes for the mental health and well-being of children in adoption and foster care, there is relatively limited evidence of effective interventions specifically for these families. Additionally, family-based interventions not specific to the context of adoption and foster-care typically show small to medium effects, and even where interventions are efficacious, not all children benefit. One explanation for why interventions may not work well for some is that responses to intervention may be influenced by an individual's genetic make-up. This paper summarises how genetically-informed research designs can help disentangle genetic from environmental processes underlying psychopathology outcomes for children, and how this evidence can provide improved insights into the development of more effective preventative intervention targets for adoption and foster-care families. We discuss current difficulties in translating behavioural genetics research to prevention science, and provide recommendations to bridge the gap between behavioural genetics research and prevention science, with lessons for adoption and foster-care research and practice.

Early inherited risk for anxiety moderates the association between fathers' child-centered parenting and early social inhibition.

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.

The relationship between parental depressive symptoms and offspring psychopathology: evidence from a children-of-twins study and an adoption study.

BACKGROUND: 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. METHOD: 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: 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. CONCLUSIONS: 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.

Environmental and genetic variance in children's observed and reported maladaptive behavior.

The genetic and environmental contributions to children's maladaptive behavior are assessed in a sample of 154 twin pairs (77 MZ twin pairs and 77 DZ twin pairs), who range in age from 6 to 11 years. To bridge the strengths of behavioral genetic methods and environmental assessment techniques, we use a multimethod, multimeasure approach to data collection, and analyze the data using behavioral genetic modeling techniques. Results indicate that genetic variation accounts for a majority of the variance in parent-reported child maladaptive behavior (average = 62%). One parent-report measure also suggests a smaller, significant contribution of shared environmental variance. In contrast to the parental ratings, the observational coding and global impressions of parent-twin interactive behavior suggest that shared environment is the primary source of variance accounting for parent and child maladaptive behavior. This is due, in part, to the direct influence one's interactive partner has on the expression of maladaptive behavior in an interactive setting. When controlling for the co-participant's behavior, genetic variation increases and shared environmental variation decreases.

Teacher ratings of externalizing behavior at school entry for boys and girls: similar early predictors and different correlates.

In a test of Patterson's Coercion Theory with young children, 156 children (82 boys and 74 girls) were studied to assess the extent to which parenting and child variables, assessed at 18 months, would predict teacher ratings of externalizing child behaviors at age 5. Child playgroup behavior, parent coercion during home observations, and marital status each emerged as predictors, whereas child temperament, attachment classification, and gender did not. At age 5, the correlates of externalizing behaviors differed for boys and girls. Boys rated higher on externalizing behaviors by the teachers presented many problems in the home and school, whereas externalizing girls did not. In fact, girls rated higher on externalizing behaviors performed better on an intelligence test, yet the girls perceived themselves as less competent.

Genetics of aggressive and violent behavior.

This article develops the topic of the genetics of aggressive and violent behavior from three directions. Firstly, evidence from twin, family, and adoption studies will establish the case for the importance of genetically transmitted factors in the genesis of aggressivity from childhood through adulthood. Secondly, evidence from adoption studies will be presented to show that some environmental conditions interact with genetic factors in such a way as to suggest that the development of aggressivity requires that both genetic and environmental factors be present. Thirdly, additional and direct evidence of genetic factors in aggressivity is presented from the perspective of molecular genetics, where underlying biochemical mechanisms associated with aggressivity have been found to be caused by specific genes in animal models with confirmation of similar physiologic mechanisms in humans.

Redistribution of cardiac output during localized granulomatous inflammation and the effect of methysergide in anesthetized rats.

The distribution of cardiac output (CO) to different organs and tissues was determined by the radioactive microsphere technique in anesthetized rats 3, 5, 7, and 10 days after subcutaneous implantation of carrageenan-impregnated sponges to induce granulomatous inflammation. Distribution of CO to organs which usually respond to stress (heart, spleen, adrenals) was increased during the acute-subacute inflammatory response, at the expense of the distribution to the head, brain, abdominal muscle, and hind legs. Later decreases were seen in distribution of CO to the kidneys, tail, forelegs, and urogenitals. Vascular-related skin temperature (measured by thermography) and distribution of CO to the back skin generally showed a decrease, particularly to the skin covering the granuloma. This latter decrease was reversed by systemic treatment with methysergide (40 mg/kg) which also increased distribution of CO to the head and decreased that to the liver. Most of the effects observed can be attributed to the extra burden on the circulation presented by the highly vascularized granuloma tissue and/or to the release of 5-hydroxytryptamine, but may differ from changes in conscious rats.

Development of enhanced blood flow responses to prostaglandin E1 in carrageenan-induced granulation tissue.

The distribution of cardiac output (c.o.) was measured by the radioactive microsphere method in rats at different time intervals after the implantation of carrageenan-impregnated sponges. The amount of blood distributed to the developing granulomata increased from day 5 after sponge implantation to day 7, but showed no further increase at day 10. A similar pattern in blood flow was observed in the skin covering the granulomata. Injection of PGE1 (100 Ng) into the sponges led to an increase in blood flow, the magnitude of which became gradually larger between days 5 and 10. A similar, though less marked increase in sensitivity to PGE1 was observed in the skin covering the granulomata, PGE1 causing a significant increase in blood flow to the skin on day 10. These changes in sensitivity to exogenous PGE1 may be due to decreasing levels of endogenous PGE and/or maturation of the newly formed blood vessels in the granulation tissue.