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Grounded on Belsky's process model and family systems theories and using an actor-partner interdependency modeling (APIM) approach (Belsky & Jaffee, 2006; Cox & Paley, 2003), the current study was the first to examine whether Big Five personality characteristics and depressive symptoms of parents and their partners are related to adolescent-perceived parenting behavior directly and indirectly via interparental stress experienced by both parents. Longitudinal data (Time 1: 2001; Time 2: 2007; and Time 3: 2009) from a large community sample of Flemish families was used (N = 455; Time 1 children: Mage = 7.10 years). Results revealed that, for both parents, more agreeableness and autonomy predicted more parental warmth, and more depressive symptoms and lower agreeableness predicted more overreactive discipline (i.e., actor effects). Both parents' depressive symptoms predicted their own interparental stress (i.e., actor effects). Regarding partner-effects, paternal overreactive discipline was shaped by mother's extraversion and experienced interparental stress, and paternal warmth was affected by mother's experienced interparental stress in addition to fathers' own psychological resources. In contrast, maternal parenting was affected by their own psychological resources only. Although no consistent mediating role of interparental stress was found, one small dyadic indirect effect indicated that maternal depressive symptoms were related to more paternal overreactive discipline via heightened levels of interparental stress experienced by both parents. These results provide new support for the idea of interdependency between parents and specifically support the fathering vulnerability hypothesis. Tentatively, this study informs clinical practice by showing that family interventions aiming to improve parenting should pay attention to specific personality characteristics affecting parenting behavior and adopt a dyadic approach including both parents, especially when targeting paternal parenting. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

According to prominent models of child development, parental factors may contribute to individual differences in children's executive functioning (EF). Here, we examine the relative importance of parents' socio-economic status, mental health, and parenting as predictors of EF development, drawing on a large (n = 1,070) community sample of Norwegian children who received biennial EF assessments from 6 to 10 years of age. We measure EF by means of the Behavior Rating Inventory of Executive Function. We assess parenting through observer ratings of parent-child interactions and parental mental health via the Beck Anxiety Inventory, Beck Depression Inventory, and Hopkins Symptom Checklist. When we adjust for all time-invariant unmeasured confounders, higher parental education predicts superior EF development, whereas harsh parenting forecasts poorer EF development. However, parenting does not mediate the effect of parental education. These results indicate that harsh parenting should be targeted in interventions aimed at improving EF. Statement of contribution What is already known on this subject? Parental factors seem to affect child development of executive functions (EF). Specifically, parental socio-economic status, mental health, and their parenting seem to influence the developmental course of child EF. What does this study add? To what degree the parental influence on EF development is likely to be driven by time-invariant factors, for example, genetics. The relative influence of positive and negative parenting on EF development.

Separate fields of inquiry indicate (a) that prenatal stress is associated with heightened behavioral and physiological reactivity and (b) that these postnatal phenotypes are themselves associated with increased susceptibility to both positive and negative environmental influences. Collectively, this work supports Pluess and Belsky's (Psychopathology, 2011, 23, 29) claim that prenatal stress fosters, promotes or "programs" postnatal developmental plasticity. Herein, we review animal and human evidence consistent with this hypothesis before advancing the novel idea that infant intestinal microbiota may be one candidate mechanism for instantiating developmental plasticity as a result of prenatal stress. We then review research indicating that prenatal stress predicts differences in infant intestinal microbiota; that infant intestinal microbiota is associated with behavioral and physiological reactivity phenotypes; and, thus, that prenatal stress may influence infant intestinal microbiota in a way that results in heightened physiological and behavioral reactivity and, thereby, postnatal developmental plasticity. Finally, we offer ideas for testing this claim and consider implications for intervention and use of probiotics during early infancy.

Young people's life chances can be predicted by characteristics of their neighbourhood1. Children growing up in disadvantaged neighbourhoods exhibit worse physical and mental health and suffer poorer educational and economic outcomes than children growing up in advantaged neighbourhoods. Increasing recognition that aspects of social inequalities tend, in fact, to be geographical inequalities2-5 is stimulating research and focusing policy interest on the role of place in shaping health, behaviour and social outcomes. Where neighbourhood effects are causal, neighbourhood-level interventions can be effective. Where neighbourhood effects reflect selection of families with different characteristics into different neighbourhoods, interventions should instead target families or individuals directly. To test how selection may affect different neighbourhood-linked problems, we linked neighbourhood data with genetic, health and social outcome data for >7,000 European-descent UK and US young people in the E-Risk and Add Health studies. We tested selection/concentration of genetic risks for obesity, schizophrenia, teen pregnancy and poor educational outcomes in high-risk neighbourhoods, including genetic analysis of neighbourhood mobility. Findings argue against genetic selection/concentration as an explanation for neighbourhood gradients in obesity and mental health problems. By contrast, modest genetic selection/concentration was evident for teen pregnancy and poor educational outcomes, suggesting that neighbourhood effects for these outcomes should be interpreted with care.

Most developmental work regards adverse developmental experiences as forces that undermine well-being. Here, I present an alternative—or complementary—view, summarizing recent evidence on puberty, endocrinology, cellular aging, and brain connectivity that collectively reveals developmental acceleration in response to contextual adversity. Findings are cast in evolutionary-developmental terms, highlighting the trade-off between accelerated aging and (a) increased morbidity and (b) premature mortality.

A recent article in this journal reported a number of gene × environment interactions involving a serotonin transporter-gene network polygenic score and a composite index of prenatal adversity predicting several problem behavior outcomes at 48 months (e.g., anxious/depressed, pervasive developmental problems) and at 60 months (e.g., withdrawal, internalizing problems), yet did not illuminate the nature or form these genetic × environment interactions took. Here we report results of six additional analyses to evaluate whether these interactions reflected diathesis-stress or differential-susceptibility related processes. Analyses of the regions of significance and proportion of interaction index are consistent with the diathesis-stress model, seemingly because of the truncated nature of the adversity score (which did not extend to supportive/positive prenatal experiences/exposures); in contrast, the proportion (of cases) affected index favors the differential-susceptibility model. These results suggest the need for future studies to extend measurement of the prenatal environment to highly supportive experiences and exposures.

The oxytocinergic system is a primary biological system involved in regulating a child's needs for bonding and for protection from threats. It is responsive to social experiences in close relationships, though evidence across studies is not entirely consistent. Guided by previous literature, we investigated individual and environmental factors predicting and presumably affecting children's oxytocin (OT) response during mother-child interaction. by focusing on children's OXTR genotype, and maternal behavior, respectively. This was achieved by assessing salivary OT levels of 88 Portuguese preschoolers prior to and following a mother-child interaction task, and by genotyping children's OXTR SNP rs53576. Maternal interactive behavior was assessed using Ainsworth scales. Results indicated that child genotype and mother's sensitive responsiveness interacted in predicting change in child OT concentrations from before to after the interaction. Specifically, Genotypic differences emerged under conditions of low maternal sensitive responsiveness: OT levels increased over time for children with the GG genotype when maternal sensitive responsiveness was low, but no such genotypic differences were evident when mothers were highly sensitive responsive. Findings provide preliminary support for the notion that increased understanding of children's OT and close relationships requires consideration of both individual and environmental factors.

Reactive Attachment Disorder (RAD) is presumed to be a consequence of social neglect and deprivation of the kind particularly associated with institutional care. Despite its clinical relevance there is a lack of assessment tools for RAD based on the direct observation of child-caregiver interaction. Here we describe the development and validation of such a tool for use with preschool children, the Rating of Inhibited Attachment Disordered Behavior (RInAB). The RInAB is composed of 17 ratings grouped in three subscales assessing (1) Attachment, (2) Exploratory, and (3) Socioemotional behavior. Participants were 134 institutionalized preschool children (M = 54.84 months; SD = 10.83; 60% boys) and their caregivers. Adequate reliability was found for RInAB subscales and total score. Confirmatory factor analyses documented the three aforementioned RInAB subscales. Correlational analyses documented: (i) construct validity via positive and significant associations with caregiver sensitivity and quality of child-caregiver relationship; (ii) convergence validity via association evidence with some emotionally/withdrawn inhibited items of the Disturbed Attachment Interview (DAI), as well as, with Child Behavior Checklist (CBCL)'s somatic complaints and withdraw syndrome scales; and (iii) discriminant validity via nonsignificant or negative associations with DAI-indiscriminate subscale, Rating of Infant and Stranger Engagement (RISE) and CBCL-externalizing problems. Discussion highlights the contributions complementary roles of RInAB for a comprehensive assessment of child RAD-related functioning.

Internet gaming disorder (IGD) was included in the Addendum to DSM-5 as a condition for further study. Studies of community samples using a diagnostic interview are lacking, and evaluations of the proposed symptoms, comorbidities, and predictors of IGD are scarce. To provide such information participants in a Norwegian prospective community study were assessed with a clinical interview at age 10 years. Symptoms of other psychiatric disorders were measured with the Child and Adolescent Psychiatric Assessment at ages 8 and 10 (n = 740). Children, parents, and teachers provided information on demographics, temperament, intelligence, executive functions, self-concept, social skills, victimization, emotion regulation, family climate, and parenting. Results indicated that IGD was present in 1.7% (95% confidence interval, 0.7-2.7) of the participants (3.0% boys and 0.5% girls). Factor analysis revealed two factors: heavy involvement and negative consequences. The positive predictive value of withdrawal, tolerance, and unsuccessful attempts to control gaming symptoms to the disorder was low. Symptoms of other common disorders correlated weakly with IGD-symptoms (i.e., from r = 0.07 to r = 0.15). Upon adjusting for gender and gaming at age 8, only limited social and emotion regulation skills at age 8 predicted more age-10 IGD symptoms. In conclusion, IGD is already present in a small percentage of Norwegian 10-year olds. At least three of the proposed symptoms -- withdrawal, tolerance and unsuccessful attempts to control gaming -- merit further study given their weak associations with the disorder. Symptoms of IGD are only marginally associated with symptoms of other psychiatric disorders and only predicted by social skills and emotion regulation deficits.

ObjectiveFrequent co-occurrence and bidirectional longitudinal associations have led some researchers to question the boundaries between depression and anxiety. A longitudinal investigation of the interconnected symptom structure of these constructs may help determine the extent to which they are distinct, and whether this changes over development. Therefore, the present study used network analysis to examine these symptom-symptom associations developmentally from early childhood to mid-adolescence.MethodWe analyzed data from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development (N = 1,147). Depression and anxiety symptoms were assessed on 7 occasions between ages 5 and 14 years using maternal reports. Regularized partial correlation networks were constructed at each time point, and diagnostic boundaries were explored using empirical tests of network modularity (ie, clustering of symptom nodes). Nonparametric permutation tests were used to determine whether symptoms became more associated over development, and network centrality was examined to identify developmental changes in the overall importance of specific symptoms.ResultsSymptoms formed highly interconnected networks, as evidenced by strong associations between depression and anxiety symptoms and a lack of distinct clustering. There was some evidence of an increase in overall connectivity as children aged. Feeling "anxious/fearful" and "unhappy/sad" were consistently the most central symptoms over development.ConclusionMinimal clustering of nodes indicated no separation of depression and anxiety symptoms from early childhood through mid-adolescence. An increase in connectivity over development suggests that symptoms may reinforce each other, potentially contributing to the high levels of lifetime continuity of these disorders.

Two separate lines of inquiry indicate (a) that prenatal stress is associated with heightened behavioral and physiological reactivity, and (b) that these postnatal phenotypes are associated with increased susceptibility to both positive and negative developmental experiences and environmental exposures. This research considered together raises the intriguing hypothesis first advanced by Pluess and Belsky (Dev Psychopathol 23:29-38, 2011) that prenatal-stress fosters, promotes or "programs" postnatal developmental plasticity. In this paper, we review further evidence consistent with this proposition, including a novel animal study which experimentally manipulated both prenatal stress and postnatal rearing. Directions for future work focused on mechanisms mediating the plasticity-inducing effects of prenatal stress and the moderators of such effects are outlined.

This research investigates whether and how two fundamental environmental factors-harshness and unpredictability-interact in regulating child and adolescent development, informed by life-history theory and drawing on data from the National Institute of Child Health & Human Development Study of Early Child Care and Youth Development (N = 1,364). Early life harshness was operationalized as the typical level of family income-to-needs based on six repeated measurements across the first 4.5 years of life and early life unpredictability as random variation using the same family income measurements. Results revealed that children functioned most competently in the social and academic domain as kindergarteners when exposed to low environmental harshness and low unpredictability and least competently when they experienced high harshness and low unpredictability. The same interaction pattern emerged in adolescence in forecasting cognitive-academic competence and sexual behavior. Findings are discussed in terms of how reliable and unreliable environmental cues shape developmental trajectories. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Background: Genome-wide association studies (GWAS) have identified large numbers of genetic variants associated with cognition. However, little is known about how these genetic discoveries impact cognitive aging. Methods: We conducted polygenic-index (PGI) analysis of cognitive performance in n = 168 European-ancestry adults aged 20–80. We computed PGIs based on GWAS of cognitive performance in young/middle-aged and older adults. We tested associations of the PGI with cognitive performance, as measured through neuropsychological evaluation. We explored whether these associations were accounted for by magnetic resonance imaging (MRI) measures of brain-aging phenotypes: total gray matter volume (GM), cortical thickness (CT), and white matter hyperintensities burden (WMH). Results: Participants with higher PGI values performed better on cognitive tests (B = 0.627, SE = 0.196, p = 0.002) (age, sex, and principal components as covariates). Associations remained significant with inclusion of covariates for MRI measures of brain aging; B = 0.439, SE: 0.198, p = 0.028). PGI associations were stronger in young and middle-aged (age

Background: Alzheimer's disease and Alzheimer's disease related dementias (AD/ADRD) have increased in prevalence. Objective: This article describes the Add Health Parent Study (AHPS) Phase 2, a study of social, behavioral, and biological factors influencing healthy aging and risk for AD/ADRD, in a national sample of adults aged 58–90. Methods: Sample members are parents of the National Longitudinal Study of Adolescent to Adult Health (Add Health) cohort, initially interviewed in Add Health in midlife (1994-95). AHPS Phase 1 (2015–17) collected longitudinal data on a random subsample of parents and their spouse/partners, who were mostly Non-Hispanic (NH) White. AHPS Phase 2 will collect the same longitudinal socio-behavioral, and health survey data on all remaining NH Black and Hispanic parents (Black and Hispanic Supplement, BHS). Additionally, Phase 2 will collect cognitive and DNA data from AHPS Phase 1 and BHS sample parents and their current spouse/partners. Results: Funded by the National Institute on Aging, recruitment will occur between June 2025 and May 2026, producing an expected total AHPS sample of 5506 parents and their spouse/partners. Conclusions: The AHPS will be the first longitudinal cohort study powered to address multigenerational racial/ethnic disparities in AD/ADRD risk and protective factors across race/ethnic groups and socioeconomic strata. [ABSTRACT FROM AUTHOR]

Background: Extensor carpi ulnaris (ECU) subsheath injuries are an increasingly recognized cause of ulnar-sided wrist pain in elite athletes. There is a lack of surgical outcome data in elite athletes, and unique considerations exist for these patients. Methods: We performed a retrospective review of our hand center experience of 14 elite professional or collegiate athletes who prospectively underwent radially based extensor retinacular sling ECU subsheath reconstruction by 3 hand surgery-fellowship-trained surgeons between April 2011 and April 2021. Clinical, magnetic resonance imaging (MRI), and intraoperative findings were cataloged. Subgroup analyses of elite hockey players and acute subsheath injuries were also conducted. Statistical analysis was performed via a 2-tailed paired t test. Results: Mean age at the time of surgery was 21.3 years (range, 18-34). Mean time from symptom onset to surgery was 102.1 ± 110.7 days. All 14 patients underwent preoperative MRI. Five patients (35.7%) had intrinsic ECU tendinopathy, 9 patients (64.3%) had ECU tenosynovitis, 6 patients (42.9%) had triangular fibrocartilage complex tears, and 9 patients (64.3%) had ulnocarpal synovitis. Mean postoperative pain on a Visual Analog Scale was 0.25 ± 0.43. Grip strength (P =.001), wrist flexion-extension (P =.037), and pronosupination arcs (P =.093) showed excellent recovery postoperatively. Mean time to unrestricted return to sports was 92.5 ± 21.0 days. There were no complications. Subgroup analyses found similar functional improvement and characterized injury patterns. Conclusions: Overall, our findings suggest surgical management of ECU subsheath injuries is a viable option in both acute and chronic settings in elite athletes and may be favorable compared with nonoperative management. [ABSTRACT FROM AUTHOR]

Twin studies have documented that parenting behavior is partly heritable, but it is unclear how parents' genetics shape their caregiving. Using tools of molecular genetics, the present study investigated this process by testing hypotheses about associations between a genome-wide polygenic score for educational attainment and parental caregiving in 702 members of the Dunedin Study, a population-representative birth cohort. Data have been prospectively collected from when Study members were born through to midlife, and include assessments of the caregiving they provided once they became parents. Results showed that parents' polygenic scores predicted warm, sensitive, and stimulating caregiving, both in personal interactions with their young children (as captured on video) and through the home environments they created for their families (as observed by home visitors). The magnitude of this effect was small. Polygenic-score associations were independent of well-established predictors of parenting, such as parents' own childhood experiences of parenting and the age at which they became parents. Polygenic-score associations were mediated by parents' early-emerging cognitive abilities and self-control skills. Findings have implications for theory and research about genetic influences on caregiving and child development.

Telomeres are the protective DNA-protein sequences appearing at the ends of chromosomes; they shorten with each cell division and are considered a biomarker of aging. Shorter telomere length and greater erosion have been associated with compromised physical and mental health and are hypothesized to be affected by early life stress. In the latter case, most work has relied on retrospective measures of early life stressors. The Dutch research (n = 193) presented herein tested 3 hypotheses prospectively regarding effects of sensitive-insensitive parenting during the first 2.5 years on telomere length at age 6, when first measured, and change over the following 4 years. It was predicted that (1) less sensitive parenting would predict shorter telomeres and greater erosion and that such effects would be most pronounced in children (2) exposed to prenatal stress and/or (3) who were highly negatively emotional as infants. Results revealed, only, that prenatal stress amplified parenting effects on telomere change--in a differential-susceptibility-related manner: Prenatally stressed children displayed more erosion when they experienced insensitive parenting and less erosion when they experienced sensitive parenting. Mechanisms that might initiate greater postnatal plasticity as a result of prenatal stress are highlighted and future work outlined.

Emerging evidence suggests that prenatal stress does not solely undermine child functioning but increases developmental plasticity to both negative and positive postnatal experiences. Here we test this proposition using the Norwegian Mother and Child Cohort study while implementing an extreme-group (i.e., high vs. low prenatal stress) design (n = 27,889 children for internalizing and n = 27,892 for externalizing problems). To measure prenatal stress, mothers reported on depressive and anxiety symptoms at gestational weeks 17 and 30 and of stressful life events at gestational week 30. We then evaluated whether, collectively, such prenatal stress amplified the effect of mothers' postnatal depressive and anxiety symptoms on children's internalizing and externalizing behavior problems at age 5 years. Results showed prenatal stress amplified effects of postnatal maternal depression/anxiety on child internalizing but not externalizing behavior, with some indication that this Prenatal-Stress-X-Postnatal-Maternal-Depression interaction proved more consistent with differential susceptibility than diathesis stress thinking: Children exposed to prenatal stress evinced greater internalizing problems if exposed to more postnatal maternal depressive/anxiety symptoms and, somewhat less strongly, displayed less internalizing problems if they experienced lower postnatal maternal depressive/anxiety symptoms. However, analyses using the whole sample instead of extreme groups yielded opposing results with children exposed to the least prenatal stress evincing greater sensitivity to postnatal maternal depressive/anxiety symptoms with regards to externalizing and internalizing behavior. Taken together, it appears that prenatal stress may have differing effects on plasticity depending on prenatal stress severity.

This study tested implications of new genetic discoveries for understanding the association between parental investment and children's educational attainment. A novel design matched genetic data from 860 British mothers and their children with home-visit measures of parenting: the E-Risk Study. Three findings emerged. First, both mothers' and children's education-associated genetics, summarized in a genome-wide polygenic score, were associated with parenting--a gene-environment correlation. Second, accounting for genetic influences slightly reduced associations between parenting and children's attainment--indicating some genetic confounding. Third, mothers' genetics were associated with children's attainment over and above children's own genetics, via cognitively stimulating parenting--an environmentally mediated effect. Findings imply that, when interpreting parents' effects on children, environmentalists must consider genetic transmission, but geneticists must also consider environmental transmission.

Maximizing the flow of students through the science, technology, engineering, and math (STEM) pipeline is important to promoting human capital development and reducing economic inequality. A critical juncture in the STEM pipeline is the highly cumulative sequence of secondary school math courses. Students from disadvantaged schools are less likely to complete advanced math courses. Here, we conduct an analysis of how the math pipeline differs across schools using student "polygenic scores," which are DNA-based indicators of propensity to succeed in education. We integrated genetic and official school transcript data from over 3000 European-ancestry students from U.S. high schools. We used polygenic scores as a molecular tracer to understand how the flow of students through the high school math pipeline differs in socioeconomically advantaged versus disadvantaged schools. Students with higher education polygenic scores were tracked to more advanced math already at the beginning of high school and persisted in math for more years. Analyses using genetics as a molecular tracer revealed that the dynamics of the math pipeline differed by school advantage. Compared to disadvantaged schools, advantaged schools buffered students with low polygenic scores from dropping out of math. Across all schools, even students with exceptional polygenic scores (top 2%) were unlikely to take the most advanced math classes, suggesting substantial room for improvement in the development of potential STEM talent. These results link new molecular genetic discoveries to a common target of educational-policy reforms.

Background Given evidence that parenting can influence children’s development, parenting interventions are often the strategy of choice when it comes to treating children’s disruptive behavior problems—or preventing problems from developing in the first place. What remains under appreciated, however, is that some parents appear to be more responsive to interventions to foster skilled parenting than others. Notable in this regard is the ever-increasing observational and, perhaps more importantly, experimental evidence indicating that some children prove more susceptible to parenting interventions than others. So, while the experimental evidence clearly indicates that “susceptibility factors” which children carry seem to affect their likelihood of benefiting from a parenting intervention (and other environmental influences), what remains unclear is why the parenting interventions in question prove more effective in changing the behavior of some parents more than others. Could it be as a result of their own parental characteristics? Objective The Parfective Microtrial in a randomized controlled microtrial, in which we focus not just on parental (and child) responsiveness but also on an underlying physiological mechanism hypothesized to contribute to heightened susceptibility to parenting interventions. Methods Participants are 120 families, with children aged 4–5 years, recruited from the community. Of these, 60 are randomly assigned to the “micro” intervention condition (i.e., immediate positive parenting feedback) and 60 families to the care-as-usual control condition. Assessments in both conditions will be conducted at baseline (pretest), after 2 weeks (posttest), and after 4 weeks (follow-up). Primary outcomes are the hypothesized moderating effects of physiology on the anticipated “micro” intervention effect (i.e., decrease in negative parenting behavior and/or increase in positive parenting behavior). Secondary outcomes are the observed (changes in) child behavior in response to the parenting intervention, such that those parents and children—in the same family—who manifest these physiological attributes will prove most susceptible to the beneficial effects of the intervention. Trial registration This study protocol is registered at ClinicalTrials.gov (NCT05539170).

BackgroundThe relationship between pubertal onset and tempo and pubertal growth is controversial. We hypothesized that the age at onset of girls' puberty predicts pubertal tempo and the rate of pubertal progression.MethodsWe analysed the data of 380 girls from the prospective Study of Early Child Care and Youth Development (SECCYD), who were recruited in the USA from 1991-2006 and followed from birth to age 15.5 years. We used the following indicators: thelarche age (Tanner stage B2), pubarche age (P2), menarche age (M), the age when breast (B5) and pubic hair (P5) became fully mature, pubertal growth, pubertal duration (time from B2 to B5), pubertal progression (time from B2 to M). We clustered the girls according to B2 age into early onset (EO;10.5 years).ResultsAll indicators of pubertal onset and conclusion occurred earlier in the EOs than in the LO; yet, the differences in the age at main pubertal milestones lessened as puberty progressed: two years for B2; -1.4 years for M; - one year for B5. In EO, puberty was one year (average) longer than in LO. Although EO grew 7 cm (average) more than LO, their heights at B5 were comparable. There was a significant relationship between the thelarche age and puberty tempo (r=0.23, P

To illuminate which features of an unpredictable environment early in life best forecast adolescent and adult functioning, data from two longitudinal studies were examined. After decomposing a composite unpredictability construct found to predict later development, results of both studies revealed that paternal transitions predicted outcomes more consistently and strongly than did residential or occupational changes across the first 5 years of a child's life. These results derive from analyses of the NICHD Study of Early Child Care and Youth Development, which included diverse families from 10 different sites in the United States, and from the Minnesota Longitudinal Study of Risk and Adaptation, whose participants came from one site, were disproportionately economically disadvantaged, and were enrolled 15 years earlier than the NICHD Study sample. The finding that results from both studies are consistent with evolutionary, life history thinking regarding the importance of males in children's lives makes this general, cross-study replication noteworthy.

BackgroundInsecure attachment in infancy is associated with a range of later socioemotional problems; therefore, it is important to identify at-risk children so that support can be provided. However, there are currently no well-validated brief measures of infant attachment. The aim of this study is to create a brief version of the Attachment Q-Sort (AQS), one of the gold-standard measures of attachment.MethodData was used from the National Institute of Child Health and Development Study of Child Care and Youth Development (N = 1,364). The factor structure of the AQS was explored, and Item Response Theory was used to select a reduced number of items. Convergent validity of the shortened measure was assessed through associations with the Strange Situation Procedure. Correlations with sensitivity, externalising, and social competence were also examined.ResultsThe Brief Attachment Scale (BAS-16) was created consisting of two scales of eight items, relating to (a) harmonious interaction with the caregiver and (b) proximity-seeking behaviours. The BAS-16 showed comparable convergent, discriminant, and concurrent validity to the full AQS.ConclusionThis brief version of the AQS shows potential as a screening measure for insecure attachment in infancy. Further development and validation is required in separate samples.

Children from some demographic groups disproportionately receive special education (SE) services. Due to methodological shortcoming in existing work, it remains unclear whether this is due to real differences in academic needs or cultural selection/bias. Hence, in a community sample of 1250 Norwegian children, we examined the role of third grade SE services, academic test scores, behavioural problems, and teacher’s level of helplessness in mediating the effect of family socio-economic status (SES) and students’ gender on fifth-grade SE services. Results revealed no direct effects of either gender or SES on fifth-grade SE, but four mediated pathways were identified: (1) Boys had a greater likelihood of receiving fifth-grade SE services when (a) they previously received SE and (b) they experienced more ADHD symptoms, both in third grade. (2) Students from low-SES families were more likely to receive SE services in fifth grade when (a) they performed poorly in math in third grade and (b) their teacher reported greater feelings of helplessness when teaching these students. The findings are discussed with respect to the differential-needs hypothesis, mechanisms of cultural selection and the possibility of gendered selection for SE at younger ages.

Two sets of evidence reviewed herein, one indicating that prenatal stress is associated with elevated behavioral and physiological dysregulation and the other that such phenotypic functioning is itself associated with heightened susceptibility to positive and negative environmental influences postnatally, raises the intriguing hypothesis first advanced by Pluess and Belsky (2011) that prenatal stress fosters, promotes, or "programs" postnatal developmental plasticity. Here we review further evidence consistent with this proposition, including new experimental research systematically manipulating both prenatal stress and postnatal rearing. Collectively this work would seem to explain why prenatal stress has so consistently been linked to problematic development: stresses encountered prenatally are likely to continue postnatally, thereby adversely affecting the development of children programmed (by prenatal stress) to be especially susceptible to environmental effects. Less investigated are the potential benefits prenatal stress may promote, due to increased plasticity, when the postnatal environment proves to be favorable. Future directions of research pertaining to potential mechanisms instantiating postnatal plasticity and moderators of such prenatal-programming effects are outlined.

Children's eating behavior influences energy intake and thus weight through choices of type and amount of food. One type of eating behavior, food responsiveness, defined as eating in response to external cues such as the sight and smell of food, is particularly related to increased caloric intake and weight. Because little is known about the potential determinants of such behavior, we focus herein on child and parent predictors of food responsiveness in a large community sample of Norwegian 6-year-olds, followed up at ages 8 and 10. To measure children's food responsiveness, parents completed the Children's Eating Behavior Questionnaire. Potential predictors were children's inhibition and symptoms of attention-deficit/hyperactivity disorder and depression, and parents' instrumental and controlling feeding practices as well as parental restrained eating. After accounting for children's initial levels of food responsiveness within a hybrid fixed effects method that takes into consideration all unmeasured time-invariant confounders, more child attention-deficit/hyperactivity disorder symptoms and greater restrained eating by parents predicted more food responsiveness at both ages 8 and 10. These results may provide important insights for efforts to prevent overeating. (PsycINFO Database Record

BACKGROUND:Recent research indicates that the best-fitting structural model of psychopathology includes a general factor capturing comorbidity (p) and several more specific, orthogonal factors. Little is known about the stability of these factors, although two opposing developmental processes have been proposed: dynamic mutualism suggests that symptom-level interaction and reinforcement may lead to a strengthening of comorbidity (p) over time, whereas p-differentiation suggests a general vulnerability to psychopathology that gives way to increasingly distinct patterns of symptoms over time. In order to test both processes, we examine two forms of developmental stability from ages 2 to 14 years: strength (i.e., consistency in the amount of variance explained by general and specific factors) and phenotypic stability (i.e., homotypic and heterotypic continuity). METHODS:Data are from the NICHD Study of Early Child Care and Youth Development. Psychopathology symptoms were assessed nine times between ages 2 and 14 years (n = 1,253) using the Child Behavior Checklist completed by mothers. Confirmatory bifactor modeling was used to test structural models of psychopathology at each age. Consistency in strength was examined by calculating the Explained Common Variance (ECV) and phenotypic stability was investigated with cross-lagged modeling of the general and specific factors. RESULTS:Bifactor models fit the data well across this developmental period. ECV values were reasonably consistent across development, with the general factor accounting for the majority of shared variance (61%-71%). Evidence of both homotypic and heterotypic continuity emerged, with most heterotypic continuity involving the general factor, as it both predicted and was predicted by specific factors. CONCLUSIONS:A bifactor model effectively captures psychopathological comorbidity from early childhood through adolescence. The longitudinal associations between the general and specific factors provide evidence for both the hypothesized processes (dynamic mutualism and p-differentiation) occurring through development.