Search

Attention-deficit hyperactivity disorder (ADHD) and subclinical symptoms of hyperactivity-impulsivity and inattentiveness coincide with an increased risk of peer victimization. What remains unclear are the developmental dynamics of these associations. In a sample drawn from two Norwegian birth cohorts ( n = 872; 49.94 % girls), assessed biennially from age 6 to age 14, reciprocal relations between ADHD symptoms and victimization were examined while controlling for symptoms of anxiety and depression. ADHD symptoms were assessed through clinical interviews with parents, whereas victimization was reported by teachers using questionnaires. Random-intercept cross-lagged panel modeling revealed a consistent reciprocal within-person effect of increased ADHD symptoms on victimization, and vice versa. Analyses of subdimensions of ADHD projected a consistent cross-lagged bidirectional relationship between victimization and inattentiveness symptoms only, whereas no such reciprocity was found for hyperactivity-impulsivity symptoms. Results did not differ by gender. Findings suggest that the social context may constitute a vulnerability factor in the etiology of the inattentive subtype of ADHD, and at the same time, that inattentiveness symptoms pose a risk for becoming victimized.

Two perspectives on the nature of nurture are reviewed, one Mendelian and the other Darwinian, in an effort to draw links between the two and, thereby, integrate them in a developmental modern synthesis, mirroring the one that took place in biology early in the last century. Thus, the heritability of environmental measures and gene-X-environment interaction are discussed with respect to Mendelian nature before turning attention to Darwinian nature and thus the development of reproductive strategies and differential susceptibility to environmental influences. Conclusions are drawn with respect to both frameworks indicating that it is time to abandon the biology-is-destiny resistance to both approaches to studying and thinking about development, especially when it comes to the nature of nurture. Implications for the future development of the field of developmental psychopathology are highlighted.

The aim of this study was to use longitudinal population-based data to examine the associations between childhood sexual abuse (CSA) and risk for adverse outcomes in multiple life domains across adulthood. In 937 individuals followed from birth to age 45y, we assessed associations between CSA (retrospectively reported at age 26y) and the experience of 22 adverse outcomes in seven domains (physical, mental, sexual, interpersonal, economic, antisocial, multi-domain) from young adulthood to midlife (26 to 45y). Analyses controlled for sex, socioeconomic status, prospectively reported child harm and household dysfunction adverse childhood experiences, and adult sexual assault, and considered different definitions of CSA. After adjusting for confounders, CSA survivors were more likely than their peers to experience internalizing, externalizing, and thought disorders, suicide attempts, health risk behaviors, systemic inflammation, poor oral health, sexually transmitted diseases, high-conflict relationships, benefit use, financial difficulties, antisocial behavior, and cumulative problems across multiple domains in adulthood. In sum, CSA was associated with multiple persistent problems across adulthood, even after adjusting for confounding life stressors, and the risk for particular problems incremented with CSA severity. The higher risk for most specific problems was small to moderate, but the cumulative long-term effects across multiple domains reflect considerable individual and societal burden.

This study focused on generality versus specificity of susceptibility of effects of eight family and child-care exposures measured between 3 and 54 months of age (e.g., sensitive parenting, child-care quality) on five child development outcomes assessed at age 4.5 years (e.g. behavior problems, preacademic skill), using data from The National Institute of Child Health and Human Development (NICHD) Study of Early Child Care and Youth Development ( n = 1,364, boys = 705; White = 1,097, Black = 176, other = 91), while applying a novel influence-statistics method. Results indicated that susceptibility across the environment-predictor:child-outcome associations is normally rather than bimodally (i.e., orchid-dandelion) distributed. Analysis of susceptibility documents both domain generality and specificity of developmental plasticity, with effect sizes proving small in the former case. As predicted, children who as infants had difficult temperaments or who scored higher on a polygenic-plasticity score (serotonin-transporter-linked promoter region [ 5-HTTLPR ], dopamine receptor D4 [ DRD4 ], brain-derived neurotrophic factor [ BDNF ]) proved somewhat more susceptible to some of the environmental effects investigated. Results lead to the recommendation that two-types-of-individuals vis-a-vis susceptibility to environmental influences be questioned and general-trait conceptions of susceptibility be further investigated.

Differential susceptibility theory stipulates that some children are more susceptible than others to both supportive and adverse developmental experiences/exposures. What remains unclear is whether the same individuals are most affected by different exposures (i.e., domain general vs. specific). We address this issue empirically for the first time using, for illustrative and proof-of-principle purposes, a novel influence-statistics' method with data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care. Results indicated that previously documented effects of greater quality of care on enhanced pre-academic skills and greater quantity of care on more behavior problems apply mostly to different children. Analyses validating the new method indicated, as predicted, that (a) the quantity-of-care effect applied principally to children from more socioeconomically advantaged families and that (b) being highly susceptible to both, one or neither childcare effect varied as a function of a three-gene, polygenic-plasticity score (serotonin transporter linked polymorphic region [ 5-HTTLPR ], dopamine receptor D4 [DRD4] , brain-derived neurotrophic factor [ BDNF ]) in a dose-response manner (i.e., 2>1>0). While domain-specific findings involving child-care effects cannot be generalized to other environmental influences, the influence-statistics' approach appears well suited for investigating the generality-specificity of environment effects, that is, of "differential, differential susceptibility."

Here we evaluate whether infant difficult temperament (6 months) functions as a vulnerability or more general plasticity factor when investigating effects of early-childhood parenting (8-42 months) on both positive and negative early-adolescent socioemotional development (age 8-11 years). Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC, N = 14,541) and a re-parameterized model-testing approach to distinguish alternative person × environment conceptual models, results indicated that temperament × parenting interacted in predicting externalizing (i.e., hyperactivity, conduct problems), but not other behavior (i.e., emotional symptoms, peer problems), in a (weak) differential susceptibility manner. While more and less supportive parenting predicted, respectively, fewer and more behavior problems, it did so more strongly for children who were more difficult as infants.

Recent dimensional models of adversity informed by a neurobiological deficit framework highlights threat and deprivation as core dimensions, whereas models informed by an evolutionary, adaptational and functional framework calls attention to harshness and unpredictability. This report seeks to evaluate an integrative model of threat, deprivation, and unpredictability, drawing on the Fragile Families Study. Confirmatory factor analysis of presumed multiple indicators of each construct reveals an adequate three-factor structure of adversity. Theory-based targeted predictions of the developmental sequelae of each dimension also received empirical support, with deprivation linked to health problems and cognitive ability; threat linked to aggression; and unpredictability to substance use and sexual risk-taking. These findings lend credibility to utility of the three-dimensional integrative framework of adversity. It could thus inform development of dimensional measures of risk assessment and exploration of multidimensional adversity profiles, sensitive to individual differences in lived experiences, supporting patient-centered, strength-based approaches to services.

Drawing on data from the Early Childhood Longitudinal Study-Birth Cohort ( n = 10,700), we evaluate indirect effects - via parent negative psychology and harsh-inconsistent parenting - of income harshness, unpredictability, and their interaction on kindergarteners' socioemotional development. Income harshness is operationalized as the typical level of family income-to-needs across four repeated measurements from 9 months to kindergarten and unpredictability as random variation across the same repeated measurements. Results indicate that the effects of greater income harshness and the harshness-X-unpredictability interaction (reflecting more predictable income harshness) on more "problematic" child behavior operated via both parent negative psychology (i.e., greater psychological stress) and harsh-inconsistent parenting. Results underscore the utility of simultaneously investigating effects of income harshness and unpredictability, as well as their interaction and mechanisms of influence.

Differential susceptibility theory stipulates that individuals vary in their susceptibility to environmental effects, often implying that the same individuals differ in the same way in their susceptibility to different environmental exposures. The latter point is addressed herein by evaluating the extent to which early-life harshness and unpredictability affect mother's psychological well-being and parenting, as well as their adolescent's life-history strategy, as reflected in number of sexual partners by age 15 years, drawing on data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care and Youth Development. Results indicated that mothers whose well-being and parenting proved more susceptible to harshness also proved somewhat more susceptible to environmental unpredictability, with the same being true of adolescent sexual behavior. Nevertheless, findings caution against overgeneralizing sample-level findings to all individuals.

Two extant frameworks - the harshness-unpredictability model and the threat-deprivation model - attempt to explain which dimensions of adversity have distinct influences on development. These models address, respectively, why, based on a history of natural selection, development operates the way it does across a range of environmental contexts, and how the neural mechanisms that underlie plasticity and learning in response to environmental experiences influence brain development. Building on these frameworks, we advance an integrated model of dimensions of environmental experience, focusing on threat-based forms of harshness, deprivation-based forms of harshness, and environmental unpredictability. This integrated model makes clear that the why and the how of development are inextricable and, together, essential to understanding which dimensions of the environment matter. Core integrative concepts include the directedness of learning, multiple levels of developmental adaptation to the environment, and tradeoffs between adaptive and maladaptive developmental responses to adversity. The integrated model proposes that proximal and distal cues to threat-based and deprivation-based forms of harshness, as well as unpredictability in those cues, calibrate development to both immediate rearing environments and broader ecological contexts, current and future. We highlight actionable directions for research needed to investigate the integrated model and advance understanding of dimensions of environmental experience.

Some Gene × Environment interaction (G×E) research has focused upon single candidate genes, whereas other related work has targeted multiple genes (e.g., polygenic scores). Each approach has informed efforts to identify individuals who are either especially vulnerable to the negative effects of contextual adversity (diathesis stress) or especially susceptible to both positive and negative contextual conditions (differential susceptibility). A critical step in all such molecular G×E research is the selection of genetic variants thought to moderate environmental influences, a subject that has not received a great deal of attention in critiques of G×E research (beyond the observation of small effects of individual genes). Here we conceptually distinguish three phases of G×E work based on the selection of genes presumed to moderate environmental effects and the theoretical basis of such decisions: (a) single candidate genes, (b) composited (multiple) candidate genes, and (c) GWAS-derived polygenic scores. This illustrative, not exhaustive, review makes it clear that implicit or explicit theoretical assumptions inform gene selection in ways that have not been clearly articulated or fully appreciated.

Currently, two main approaches exist to distinguish differential susceptibility from diathesis-stress and vantage sensitivity in Genotype × Environment interaction (G × E) research: regions of significance (RoS) and competitive-confirmatory approaches. Each is limited by its single-gene/single-environment foci given that most phenotypes are the product of multiple interacting genetic and environmental factors. We thus addressed these two concerns in a recently developed R package (LEGIT) for constructing G × E interaction models with latent genetic and environmental scores using alternating optimization. Herein we test, by means of computer simulation, diverse G × E models in the context of both single and multiple genes and environments. Results indicate that the RoS and competitive-confirmatory approaches were highly accurate when the sample size was large, whereas the latter performed better in small samples and for small effect sizes. The competitive-confirmatory approach generally had good accuracy (a) when effect size was moderate and N ≥ 500 and (b) when effect size was large and N ≥ 250, whereas RoS performed poorly. Computational tools to determine the type of G × E of multiple genes and environments are provided as extensions in our LEGIT R package.

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.

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.

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.

A wealth of evidence documents associations between various aspects of the rearing environment and later development. Two evolutionary-inspired models advance explanations for why and how such early experiences shape later functioning: (a) the external-prediction model, which highlights the role of the early environment (e.g., parenting) in regulating children's development, and (b) the internal-prediction model, which emphasizes internal state (i.e., health) as the critical regulator. Thus, by using data from the NICHD Study of Early Child Care and Youth Development, the current project draws from both models by investigating whether the effect of the early environment on later adolescent functioning is subject to an indirect effect by internal-health variables. Results showed a significant indirect effect of internal health on the relation between the early environment and adolescent behavior. Specifically, early environmental adversity during the first 5 years of life predicted lower quality health during childhood, which then led to problematic adolescent functioning and earlier age of menarche for girls. In addition, for girls, early adversity predicted lower quality health that forecasted earlier age of menarche leading to increased adolescent risk taking. The discussion highlights the importance of integrating both internal and external models to further understand the developmental processes that effect adolescent behavior.

Two independent lines of inquiry suggest that growing up under conditions of contextual adversity (e.g., poverty and household chaos) accelerates aging and undermines long-term health. Whereas work addressing the developmental origins of health and disease highlights accelerated-aging effects of contextual adversity on telomere erosion, that informed by an evolutionary analysis of reproductive strategies highlights such effects with regard to pubertal development (in females). That both shorter telomeres early in life and earlier age of menarche are associated with poor health later in life raises the prospect, consistent with evolutionary life-history theory, that these two bodies of theory and research are tapping into the same evolutionary-developmental process whereby longer term health costs are traded off for increased probability of reproducing before dying via a process of accelerated aging. Here we make the case for such a claim, while highlighting biological processes responsible for these effects, as well as unknowns in the epigenetic equation that might instantiate these contextually regulated developmental processes.

Individuals with the short variant of the serotonin transporter linked polymorphic region gene are more susceptible than individuals homozygous for the long allele to the effects of stressful life events on risk for internalizing and externalizing problems. We tested whether individual differences in coping style explained this increased risk for problem behavior among youth who were at both genetic and environmental risk. Participants included 279 children, ages 8-11, from the Children's Experiences and Development Study. Caregivers and teachers reported on children's internalizing and externalizing symptoms, and caregivers and children on children's exposure to harsh parenting and parental warmth in middle childhood, and traumatic events. Children reported how frequently they used various coping strategies. Results revealed that short/short homozygotes had higher levels of internalizing problems compared with long allele carriers and that short allele carriers had higher levels of externalizing problems compared with long/long homozygotes under conditions of high cumulative risk. Moreover, among children who were homozygous for the short allele, those who had more cumulative risk indicators less frequently used distraction coping strategies, which partly explained why they had higher levels of internalizing problems. Coping strategies did not significantly mediate Gene × Environment effects on externalizing symptoms.

Evocative effects of child characteristics on the quality and quantity of child care were assessed in two studies using longitudinal data from the NICHD Study of Early Child Care. We focus on the influence of child characteristics on two important aspects of the child care experience: language stimulation provided by caregivers and quantity of care. In Study 1, associations between the developmental status of children aged 15 to 54 months and the language stimulation provided by their caregivers were examined using path models, and longitudinal child effects were detected across the earliest time points of the study. In Study 2, the associations among child behavior, temperament, development, and time in care were examined. Little evidence was found for such child effects on time in care. The results are discussed in terms of the effects of child care on child development and implications for developmental processes, particularly for children at greatest risk for developmental delay or psychopathology.

Here we tested whether there was genetic moderation of effects of early maternal sensitivity on social-emotional and cognitive-linguistic development from early childhood onward and whether any detected Gene × Environment interaction effects proved consistent with differential-susceptibility or diathesis-stress models of Person × Environment interaction (N = 695). Two new approaches for evaluating models were employed with 12 candidate genes. Whereas maternal sensitivity proved to be a consistent predictor of child functioning across the primary-school years, candidate genes did not show many main effects, nor did they tend to interact with maternal sensitivity/insensitivity. These findings suggest that the developmental benefits of early sensitive mothering and the costs of insensitive mothering look more similar than different across genetically different children in the current sample. Although acknowledgement of this result is important, it is equally important that the generally null Gene × Environment results reported here not be overgeneralized to other samples, other predictors, other outcomes, and other candidate genes.

Manuck, Craig, Flory, Halder, and Ferrell (2011) reported that a theoretically anticipated effect of family rearing on girls' menarcheal age was genetically moderated by two single nucleotide polymorphisms (SNPs) of the estrogen receptor-α gene. We sought to replicate and extend these findings, studying 210 White females followed from birth. The replication was general because a different measure of the rearing environment was used in this inquiry (i.e., maternal sensitivity) than in the prior one (i.e., family cohesion). Extensions of the work included prospective rather than retrospective measurements of the rearing environment, reports of first menstruation within a year of its occurrence rather than decades later, accounting for some heritability of menarcheal age by controlling for maternal age of menarche, and using a new model-fitting approach to competitively compare diathesis-stress versus differential-susceptibility models of Gene × Environment interaction. The replication/extension effort proved successful in the case of both estrogen receptor-α SNPs, with the Gene × Environment interactions principally reflecting diathesis-stress: lower levels of maternal sensitivity predicted earlier age of menarche for girls homozygous for the minor alleles of either SNP but not for girls carrying other genotypes. Results are discussed in light of the new analytic methods adopted.

Background: Recently, a general psychopathology dimension reflecting common aspects among disorders has been identified in adults. This has not yet been considered in children and adolescents, where the focus has been on externalising and internalising dimensions., Aims: To examine the existence, correlates and predictive value of a general psychopathology dimension in young people., Method: Alternative factor models were estimated using self-reports of symptoms in a large community-based sample aged 11-13.5 years (N = 23 477), and resulting dimensions were assessed in terms of associations with external correlates and future functioning., Results: Both a traditional two-factor model and a bi-factor model with a general psychopathology bi-factor fitted the data well. The general psychopathology bi-factor best predicted future psychopathology and academic attainment. Associations with correlates and factor loadings are discussed., Conclusions: A general psychopathology factor, which is equal across genders, can be identified in young people. Its associations with correlates and future functioning indicate that investigating this factor can increase our understanding of the aetiology, risk and correlates of psychopathology., (© The Royal College of Psychiatrists 2015.)

Children with histories of disorganized attachment exhibit diverse problems, possibly because disorganization takes at least two distinctive forms as children age: controlling-punitive and controlling-caregiving. This variation in the developmental legacy of disorganization has been attributed primarily to variations in children's rearing experiences. Here an alternative explanation of these divergent sequelae of disorganization is evaluated: one focused on genotype. Structural equation modeling was applied to data on 704 Norwegian children to test whether the catechol-O-methyltransferase Val158Met genotype moderates the effect of disorganized attachment, which was measured dimensionally at 4 years of age using the Manchester Child Attachment Story Task, on changes in aggressive behavior and social competence from ages 4 to 6. Children who scored high on disorganization and were homozygous for the valine allele displayed significantly greater increases in aggression and decreases in self-oriented social skills (e.g., self-regulation and assertiveness) over time than did their disorganized counterparts carrying the methionine allele, whereas disorganized children carrying the methionine allele increased their other-oriented social skill (e.g., cooperation and responsibility) scores more than did valine-homozygous children. These results are consistent with the controlling-punitive and controlling-caregiving behaviors observed in disorganized children, suggesting that the children's genotype contributed to variations in the social development of disorganized children.

We provide a theoretical and empirical basis for the claim that individual differences exist in developmental plasticity and that phenotypic plasticity should be a subject of study in its own right. To advance this argument, we begin by highlighting challenges that evolutionary thinking poses for a science of development and psychopathology, including for the diathesis-stress framework that has (fruitfully) guided so much empirical inquiry on developmental risk, resilience, and dysregulation. With this foundation laid, we raise a series of issues that the differential-susceptibility hypothesis calls attention to, while highlighting findings that have emerged over just the past several years and are pertinent to some of the questions posed. Even though it is clear that this new perspective on Person × Environment interaction is stimulating research and influencing how hypotheses are framed and data interpreted, a great many topics remain that need empirical attention. Our intention is to encourage students of development and psychopathology to treat phenotypic plasticity as an individual-difference construct while exploring unknowns in the differential-susceptibility equation.

The effects of divorce on children's behavioral development have proven to be quite varied across studies, and most developmental and family scholars today appreciate the great heterogeneity in divorce effects. Thus, this inquiry sought to determine whether select dopaminergic genes previously associated with externalizing behavior and/or found to moderate diverse environmental effects (dopamine receptors D2 and D4, catechol-O-methyltransferase) might moderate divorce effects on adolescent self-reported externalizing problems; and, if so, whether evidence of gene-environment (G × E) interaction would prove consistent with diathesis-stress or differential-susceptibility models of environmental action. Data from the first and third wave of the Dutch Tracking Adolescents' Individual Lives Survey (n = 1,134) revealed some evidence of G × E interaction reflecting diathesis-stress but not differential susceptibility. It is intriguing that some evidence pointed to "vantage sensitivity," which are benefits accruing to those with a specific genotype when their parents remained together, the exact opposite of diathesis-stress. The limits of this work are considered, especially with regard to the conditions for testing differential susceptibility, and future directions are outlined.

Evidence indicates that maternal prenatal distress predicts problematic health and behavioral outcomes in children as well as infant/child cortisol levels and negative emotionality as reviewed here. Evidence that these physiological and behavioral characteristics themselves moderate environmental effects on development in a "for better and for worse" manner consistent with Belsky's differential susceptibility hypothesis and Boyce and Ellis' notions of biological sensitivity to context raises the prospect that susceptibility to rearing is a function of nurture (i.e., fetal environment), consistent with Boyce and Ellis' proposal that plasticity can be shaped by developmental experience. This hypothesis is supported by new findings from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development showing that low birth weight, a marker for an adverse prenatal environment, predicts infant difficult temperament, which is a susceptibility factor that we previously showed as moderating, in a for better and for worse manner, the effects of parenting and child care quality on socioemotional functioning. Moreover, recent Gene × Environment interaction research raises the prospect that some fetuses may be more susceptible to such "prenatal programming of postnatal plasticity" as a result of their genetic makeup. If this proves true, it will be consistent with the conclusion that early developmental plasticity is a function of both nature and nurture and may be evolutionarily adaptive, a further possibility considered in the discussion.

Two extant evolutionary models, biological sensitivity to context theory (BSCT) and differential susceptibility theory (DST), converge on the hypothesis that some individuals are more susceptible than others to both negative (risk-promoting) and positive (development-enhancing) environmental conditions. These models contrast with the currently dominant perspective on personal vulnerability and environmental risk: diathesis stress/dual risk. We review challenges to this perspective based on emerging theory and data from the evolutionary, developmental, and health sciences. These challenges signify the need for a paradigm shift in conceptualizing Person x Environment interactions in development. In this context we advance an evolutionary--neurodevelopmental theory, based on DST and BSCT, of the role of neurobiological susceptibility to the environment in regulating environmental effects on adaptation, development, and health. We then outline current thinking about neurogenomic and endophenotypic mechanisms that may underpin neurobiological susceptibility, summarize extant empirical research on differential susceptibility, and evaluate the evolutionary bases and implications of BSCT and DST. Finally, we discuss applied issues including methodological and statistical considerations in conducting differential susceptibility research; issues of ecological, cultural, and racial--ethnic variation in neurobiological susceptibility; and implications of differential susceptibility for designing social programs. We conclude that the differential susceptibility paradigm has far-reaching implications for understanding whether and how much child and adult development responds, for better and for worse, to the gamut of species-typical environmental conditions.

Teacher-rated trajectories of physical aggression in boys and girls from first through sixth grade were examined using data from the NICHD Study of Early Child Care and Youth Development. In separate analyses, four trajectories were identified in boys and three in girls. Higher levels of aggression in both boys and girls were related to greater sociodemographic risk and higher maternal harshness in the preschool years; lower levels of observed maternal sensitivity during early childhood also predicted higher trajectories of aggression among girls. Trajectory groups also differed on a range of social and academic adjustment outcomes in sixth grade, with the most aggressive children and even moderately aggressive children evidencing some difficulties in adjustment. Patterns and levels of aggression in boys and girls are discussed as are their predictors and consequences.

To identify types of families, latent-class analysis was applied to (reported) marriage and (observed) parenting measures obtained during the infancy, toddler, and/or preschool years for 828 two-parent families participating in the NICHD Study of Child Care. Five types of families were identified: Consistently Supportive (i.e., good parenting, good marriage, 15% of sample), Consistently Moderate (i.e., moderate marriage, moderate parenting. 43%), Consistently Risky (i.e., poor parenting, poor marriage, 16%), Good Parenting/Poor Marriage (19%), and Poor Parenting/Good Marriage (7%). When groups were compared in terms of contextual antecedents (measured at child age 1 month) and child cognitive-academic and socioemotional functioning in first grade, results indicated (a) that contextual risks increased linearly and children's functioning decreased linearly as one moved across the first three aforementioned groups; and after controlling for group differences in background factors (b) that children in the Good-Parenting/Poor-Marriage families outperformed those in the Poor Parenting/Good Marriage; (c) that there was evidence of "added value" developmentally when children experienced two sources of support (i.e., good marriage and good parenting) rather than just one (i.e., good marriage or good parenting); but (d) that there was only modest evidence of protective buffering whereby children experiencing just good parenting (but not just good marriages) outperformed children experiencing poor parenting and poor marriages. Results are discussed in terms of the relative influence of marriage and parenting on child development and the potential benefits of applying typological approaches to the study of marriage-parenting family subsystems.

In light of evidence that the effects of attachment security on subsequent development may be contingent on the social context in which the child continues to develop, we examined the effect of attachment security at age 15 months, cumulative contextual risk from 1 to 36 months, and the interaction of attachment and cumulative risk to predict socioemotional and cognitive linguistic functioning at age 3 years, using data from the National Institute of Child Health and Human Development Study of Early Child Care. Results indicated that early attachment predicts both socioemotional development and language skills, but not cognitive functioning as indexed by a measure of school readiness, and that the effect of attachment on socioemotional development and expressive language varied as a function of social-contextual risk. Insecure-avoidant infants proved most vulnerable to contextual risk, not children classified as secure or insecure more generally, although in one instance security did prove protective with respect to the adverse effects of cumulative contextual risk. Findings are discussed in terms of risk and resilience and in light of the probabilistic nature of the relation between early attachment and later development.

This 20-year longitudinal study showed that the young adult offspring of teen mothers are at risk for a range of adverse outcomes including early school leaving, unemployment, early parenthood, and violent offending. We tested how much the effect of teen childbearing on offspring outcomes could be accounted for by social selection (in which a woman's characteristics that make her an inadequate parent also make her likely to bear children in her teens) versus social influence (in which the consequences of becoming a teen mother also bring harm to her children, apart from any characteristics of her own). The results provided support for both mechanisms. Across outcomes, maternal characteristics and family circumstances together accounted for approximately 39% of the effect of teen childbearing on offspring outcomes. Consistent with a social-selection hypothesis, maternal characteristics accounted for approximately 18% of the effect of teen childbearing on offspring outcomes; consistent with a social-influence hypothesis, family circumstances accounted for 21% of the teen childbearing effect after controlling for maternal characteristics. These results suggest that public policy initiatives should be targeted not only at delaying childbearing in the population but at supporting individual at-risk mothers and their children.

Research suggests that adults who have developed a coherent perspective on their negative, early attachment relationships (i.e., earned secures) do not reenact poor parenting practices with their own children. However, no studies have addressed whether earned secures maintain positive parenting under the pressures of aversive environmental conditions. This study tested five alternative models that predict how earned secures parent under low and high stress in comparison to adults who had a positive upbringing (i.e., continuous secures) and adults who have an incoherent perspective on a troubled childhood (i.e., insecures). Only if earned secures exhibit effective caregiving under high stress, in comparison to the other security groups, can it be assumed that they have broken the intergenerational cycle of poor parenting. The Adult Attachment Interview was used to classify 97 mothers as earned secure, continuous secure, and insecure. Home observations of parenting and maternal self-reports of daily hassles (our stress measure) were obtained when children were 27 months old. Planned comparisons revealed that the diathesis-stress/incoherent present state of mind model most accurately predicted parenting. Thus, under high stress, the earned secures parented equivalently to the continuous secures and more positively than the insecures; under low stress no group differences were obtained. These findings indicate that in a normative sample earned secures break the intergenerational cycle and exhibit resilient parenting even under high stress conditions.

To examine the effects of infant negative emotionality and of mothering and fathering during the toddler years on 3-year-old boys' externalizing problems and inhibition, as well as explore the proposition that children vary in their susceptibility to rearing influence, 125 first-born, Caucasian boys from maritally intact families were studied. Results revealed that when infant negativity is measured with objective, replicable, and discriminantly valid procedures, no relation obtains between it and externalizing problems (nor inhibition). Moreover, as hypothesized on the basis of prior work, parenting was a stronger predictor of externalizing problems and inhibition in the case of children who were highly negative as infants. Mothering proved a stronger predictor of externalizing problems and fathering of inhibition, with more negative mothering in the 2nd and 3rd year forecasting higher CBCL-externalizing scores and less negative fathering in the 2nd and 3rd year and more positive fathering in the 2nd year forecasting more inhibition at age 3 Implications of these findings for studies of parental influence are considered.