Although allostatic load has been investigated in mood and anxiety disorders, no prior study has investigated developmental change in allostatic load as a precursor to schizotypal personality. This study employed a multilevel developmental framework to examine whether the development of increased allostatic load, as indicated by impaired sympathetic nervous system habituation from ages 3 to 11 years, predisposes to schizotypal personality at age 23 years. Electrodermal activity to six aversive tones was recorded in 995 subjects at age 3 years and again at 11 years. Habituation slopes at both ages were used to create groups who showed a developmental increase in habituation (decreased allostatic load), and those who showed a developmental decrease in habituation (increased allostatic load). Children who showed a developmental increase in allostatic load from ages 3 to 11 years had higher levels of schizotypal personality at 23 years. A breakdown of total schizotypy scores demonstrated specificity of findings to cognitive–perceptual features of schizotypy. Findings are the first to document a developmental abnormality in allostasis in relation to adult schizotypal personality. The relative failure to develop normal habituation to repeated stressors throughout childhood is hypothesized to result in an accumulation of allostatic load and consequently increased positive symptom schizotypy in adulthood.

Allostatic load theory hypothesizes that stress and the body's responses to stressors contribute to longer term physiological changes in multiple systems over time (allostasis), and that shifts in how these systems function have implications for adjustment and health. We investigated these hypotheses with longitudinal data from two independent samples (n = 413; 219 girls, 194 boys) with repeated measures at ages 8, 9, 10, and 11. Initial parental marital conflict and its change over time indexed children's exposure to an important familial stressor, which was examined in interaction with children's respiratory sinus arrhythmia (RSA) reactivity to laboratory tasks (stress response) to predict children's basal levels of RSA over time. We also investigated children's sex as an additional possible moderator. Our second research question focused on examining whether initial levels and changes in resting RSA over time predicted children's externalizing behavior. Boys with a strong RSA suppression response to a frustrating laboratory task who experienced higher initial marital conflict or increasing marital conflict over time showed decreases in their resting RSA over time. In addition, boys' initial resting RSA (but not changes in resting RSA over time) was negatively related to change over time in externalizing symptoms. Findings for girls were more mixed. Results are discussed in the context of developmental psychobiology, allostatic load, and implications for the development of psychopathology.

Age at menarche, a sentinel index of pubertal maturation, was examined in relation to early family relationships (conflict, cohesion) and polymorphic variation in the gene encoding estrogen receptor-α (ESR1) in a midlife sample of 455 European American women. Consistent with prior literature, women who reported being raised in families characterized by close interpersonal relationships and little conflict tended to reach menarche at a later age than participants reared in families lacking cohesion and prone to discord. Moreover, this association was moderated by ESR1 variation, such that quality of the family environment covaried positively with menarcheal age among participants homozygous for minor alleles of the two ESR1 polymorphisms studied here (rs9304799, rs2234693), but not among women of other ESR1 genotypes. In addition, (a) family relationship variables were unrelated to ESR1 variation, and (b) genotype-dependent effects of childhood environment on age at menarche could not be accounted for by personality traits elsewhere shown to explain heritable variation in reported family conflict and cohesion. These findings are consistent with theories of differential susceptibility to environmental influence, as well as the more specific hypothesis (by Belsky) that girls differ genetically in their sensitivity to rearing effects on pubertal maturation.

The purpose of the present research was to examine Deese–Roediger–McDermott false memory for trauma-related and nontrauma-related lists in adolescents and adults with and without documented histories of child sexual abuse (CSA). Individual differences in psychopathology and adult attachment were also explored. Participants were administered free recall and recognition tests after hearing CSA, negative, neutral, and positive Deese–Roediger–McDermott lists. In free recall, CSA and negative lists produced the most false memory. In sharp contrast, for recognition, CSA lists enjoyed the highest d′ scores. CSA-group adolescents who evinced greater posttraumatic stress disorder (PTSD) symptoms had higher rates of false memory compared to (a) non-CSA group adolescents with higher PTSD symptom scores (free recall), and (b) CSA-group adolescents with lower PTSD symptom scores (recognition). Regression analyses revealed that individuals with higher PTSD scores and greater fearful-avoidant attachment tendencies showed less proficient memory monitoring for CSA lists. Implications for trauma and memory development and for translational research are discussed.

Guided by evolutionary–developmental theories of biological sensitivity to context and reproductive development, the current research examined the interactive effects of early family environments and psychobiologic reactivity to stress on the subsequent timing and tempo of puberty. As predicted by the theory, among children displaying heightened biological sensitivity to context (i.e., higher stress reactivity), higher quality parent–child relationships forecast slower initial pubertal tempo and later pubertal timing, whereas lower quality parent–child relationships forecast the opposite pattern. No such effects emerged among less context-sensitive children. Whereas sympathetic nervous system reactivity moderated the effects of parent–child relationships on both breast/genital and pubic hair development, adrenocortical activation only moderated the effect on pubic hair development. The current results build on previous research documenting what family contexts predict variation in pubertal timing by demonstrating for whom those contexts matter. In addition, the authors advance a new methodological approach for assessing pubertal tempo using piecewise growth curve analysis.

The ability to effectively regulate emotions and a secure attachment style are critical for maintaining mental health across the life span. The experience of childhood maltreatment interferes with normal development of emotional regulation and dramatically increases risk for a wide range of psychiatric disorders in adulthood. The central nervous system oxytocin systems are critically involved in mediating social attachment and buffering psychophysiological responses to stress. We therefore investigated the impact of childhood maltreatment and an oxytocin receptor (OXTR) single nucleotide polymorphism (rs53576) and their interaction on emotional dysregulation and attachment style in adulthood in a sample of low-income, African American men and women recruited from primary care clinics of an urban, public hospital. Consistent with prior research, we found that the severity of childhood maltreatment was associated with increased levels of emotional dysregulation in adulthood. Childhood maltreatment was also positively associated with ratings of disorganized/unresolved adult attachment style and negatively associated with ratings of secure adult attachment style. There was no direct association between rs53576 and emotional dysregulation or ratings of adult attachment style. However, there were significant interactions between rs53576 and childhood maltreatment in predicting level of adult emotional dysregulation and attachment style. Specifically, G/G genotype carriers were at risk for increased emotional dysregulation when exposed to three or more categories of childhood abuse. In addition, G/G genotype carriers exhibited enhanced disorganized adult attachment style when exposed to severe childhood abuse compared to A/A and A/G carriers. Our findings suggest that A allele carriers of OXTR rs53576 are resilient against the effects of severe childhood adversity, by protection against emotional dysregulation and disorganized attachment.

The present study applies an allostatic load framework to an examination of the relationship between maternal psychosocial risk factors and maladaptive parenting behaviors. Specifically, the implications of low socioeconomic status and maternal depressive symptoms for maternal sympathovagal functioning during young children's distress were examined, as well as whether that functioning was, in turn, associated with maternal insensitivity, hostility, intrusiveness, and disengagement during mother–child dyadic interaction. Consistent with an allostatic framework, three patterns of sympathovagal functioning were expected to emerge: normative arousal, hyperarousal, and hypoarousal profiles. Furthermore, meaningful associations between maternal psychosocial risk factors, maladaptive parenting behaviors, and the three profiles of sympathovagal functioning were anticipated. Participants included 153 mother–toddler dyads recruited proportionately from lower and middle socioeconomic status backgrounds. Mothers’ sympathovagal response to their child's distress was assessed during the Strange Situation paradigm, and mothers’ parenting behavior was assessed during a dyadic free-play interaction. As hypothesized, normative arousal, hyperarousal, and hypoarousal profiles of maternal sympathovagal functioning were identified. Maternal depressive symptomatology predicted the hyperarousal profile, whereas socioeconomic adversity predicted hypoarousal. Moreover, allostatic load profiles were differentially associated with problematic parenting behaviors. These findings underscore the role of physiological dysregulation as a mechanism in the relationship between proximal risk factors and actual maladaptive parenting behaviors.

Psychobiological models of allostatic load have delineated the effects of multiple processes that contribute to risk for psychopathology. This approach has been fruitful, but the interactive contributions of allostatic and environmental load remain understudied in early childhood. Because this developmental period encompasses the emergence of internalizing problems and biological sensitivity to early experiences, this is an important time to examine this process. In two studies, we examined allostatic and environmental load and links to subsequent internalizing and externalizing problems. Study 1 examined relations between load indices and maladjustment, concurrently and at multiple times between age 2 and kindergarten; Study 2 added more comprehensive risk indices in a sample following a group of highly fearful toddlers from 2 to 3 years of age. Results from both studies showed that increased allostatic load related to internalizing problems as environmental risk also increased. Study 2, in addition, showed that fearfulness interacted with allostatic and environmental load indices to predict greater anxiety among the fearful children who had high levels of allostatic and environmental load. Taken together, the findings support a model of risk for internalizing characterized by the interaction of biological and environmental stressors, and demonstrate the importance of considering individual differences and environmental context in applying models of allostatic load to developmental change in early childhood.

This is a report on the research design and findings of a 23-year longitudinal study of the impact of intrafamilial sexual abuse on female development. The conceptual framework integrated concepts of psychological adjustment with theory regarding how psychobiological factors might impact development. Participants included 6- to 16-year-old females with substantiated sexual abuse and a demographically similar comparison group. A cross-sequential design was used and six assessments have taken place, with participants at median age 11 at the first assessment and median age 25 at the sixth assessment. Mothers of participants took part in the early assessments and offspring took part at the sixth assessment. Results of many analyses, both within circumscribed developmental stages and across development, indicated that sexually abused females (on average) showed deleterious sequelae across a host of biopsychosocial domains including: earlier onsets of puberty, cognitive deficits, depression, dissociative symptoms, maladaptive sexual development, hypothalamic–pituitary–adrenal attenuation, asymmetrical stress responses, high rates of obesity, more major illnesses and healthcare utilization, dropping out of high school, persistent posttraumatic stress disorder, self-mutilation, Diagnostic and Statistical Manual of Mental Disorders diagnoses, physical and sexual revictimization, premature deliveries, teen motherhood, drug and alcohol abuse, and domestic violence. Offspring born to abused mothers were at increased risk for child maltreatment and overall maldevelopment. There was also a pattern of considerable within group variability. Based on this complex network of findings, implications for optimal treatments are elucidated. Translational aspects of extending observational research into clinical practice are discussed in terms that will likely have a sustained impact on several major public health initiatives.

Using an ethnically diverse longitudinal sample of 338 kindergarten children, this study examined the effects of cumulative contextual stressors on children's developing hypothalamic–pituitary–adrenocortical (HPA) axis regulation as an early life indicator of allostatic load. Chronic HPA axis regulation was assessed using cumulative, multiday measures of cortisol in both the fall and spring seasons of the kindergarten year. Hierarchical linear regression analyses revealed that contextual stressors related to ethnic minority status, socioeconomic status, and family adversity each uniquely predicted children's daily HPA activity and that some of those associations were curvilinear in conformation. Results showed that the quadratic, U-shaped influences of family socioeconomic status and family adversity operate in different directions to predict children's HPA axis regulation. Results further suggested that these associations differ for White and ethnic minority children. In total, this study revealed that early childhood experiences contribute to shifts in one of the principal neurobiological systems thought to generate allostatic load, confirming the importance of early prevention and intervention efforts. Moreover, findings suggested that analyses of allostatic load and developmental theories accounting for its accrual would benefit from an inclusion of curvilinear associations in tested predictive models.

Growing evidence supports the biological sensitivity to context theory, which posits that physiologically reactive children, as indexed by autonomic nervous system (ANS) reactivity to laboratory stressors, are more susceptible to both negative and positive environmental influences than their low reactive peers. High biological sensitivity is a risk factor for behavioral and health problems in the context of high adversity, whereas in contexts of low adversity it has been found to promote positive adaptation. However, several studies have shown the opposite effect, finding that children who exhibited high ANS reactivity in response to interpersonal stressors were buffered from the deleterious effects of marital conflict, whereas children who showed low ANS reactivity were more vulnerable to high levels of marital conflict. Using an ethnically diverse sample of 260 kindergartners (130 girls, 130 boys), the current study investigated whether the interaction effect of marital conflict and the two branches of ANS reactivity on children's externalizing and internalizing symptoms differs with the nature of the laboratory challenge task used to measure children's stress response. As hypothesized, results indicate that the interaction between ANS reactivity and marital conflict significantly predicted children's behavior problems, but the direction of the effect varied with the nature of the challenge task (i.e., interpersonal or cognitive). This study illustrates the importance of considering the effect of laboratory stimuli when assessing whether children's ANS reactivity moderates the effects of adversity exposure on adaptation.

This paper examined the relation of early environmental adversity associated with poverty to child resting or basal level of cortisol in a prospective longitudinal sample of 1135 children seen at 7, 15, 24, 35, and 48 months of age. We found main effects for poor housing quality, African American ethnicity, and low positive caregiving behavior in which each was uniquely associated with an overall higher level of cortisol from age 7 to 48 months. We also found that two aspects of the early environment in the context of poverty, adult exits from the home and perceived economic insufficiency, were related to salivary cortisol in a time-dependent manner. The effect for the first of these, exits from the home, was consistent with the principle of allostatic load in which the effects of adversity on stress physiology accumulate over time. The effect for perceived economic insufficiency was one in which insufficiency was associated with higher levels of cortisol in infancy but with a typical but steeper decline in cortisol with age at subsequent time points.

The goal of this study was to examine whether growth delay can serve as an index of allostatic load during early development, as it is well known that the activity of stress-mediating systems inhibits growth. The participants were children adopted internationally from institutional care (n = 36), children adopted internationally from foster care (n = 26), and nonadopted children (n = 35). For the adopted children, height for age and weight for height were assessed at adoption; for all children, disinhibited social approach (DSA; termed elsewhere as “indiscriminate friendliness”) and diurnal cortisol were assessed at 6–8 years (M = 6.9 years). For internationally adopted children in general, and postinstitutionalized children specifically, linear growth delay assessed at the time of adoption was associated with more dysregulated behavior in response to an unfamiliar adult (i.e., greater DSA) and a more dysregulated diurnal cortisol rhythm (i.e., higher late afternoon and evening values). Further, among the most growth-delayed children, higher cortisol levels later in the day were correlated with DSA. The potential for using growth delay as an allostatic load indicator and the possible problems and limitations in its use in child populations are discussed.

The effects of childhood abuse are diverse, and although pathology is not the only outcome, psychiatric illness, including posttraumatic stress disorder (PTSD), can develop. However, adult PTSD is less common among those who experienced single-event traumas as children than it is among those who experienced childhood abuse. In addition, PTSD is more common among adults than children who experienced childhood abuse. Such evidence raises doubt about the direct, causal link between childhood trauma and adult PTSD. The experience of childhood trauma, and in particular abuse, has been identified as a risk factor for subsequent development of PTSD following exposure to adult trauma, and a substantial literature identifies revictimization as a factor that plays a pivotal role in this trajectory. The literature on the developmental effects of childhood abuse and pathways to revictimization, when considered in tandem with the biological effects of early stress in animal models, may provide some explanations for this. Specifically, it seems possible that permanent sensitization of the hypothalamic–pituitary–adrenal axis and behavioral outcomes are a consequence of childhood abuse, and these combine with the impact of retraumatization to sustain, perpetuate, and amplify symptomatology of those exposed to maltreatment in childhood.

Child maltreatment and biomarkers of allostatic load were investigated in relation to child health problems and psychological symptomatology. Participants attended a summer research day camp and included 137 maltreated and 110 nonmaltreated low-income children, who were aged 8 to 10 years (M = 9.42) and racially and ethnically diverse; 52% were male. Measurements obtained included salivary cortisol and dehydroepiandosterone, body mass index, waist–hip ratio, and blood pressure; these indicators provided a composite index of allostatic load. Child self-report and camp adult-rater reports of child symptomatology were obtained; mothers provided information on health problems. The results indicated that higher allostatic load and child maltreatment status independently predicted poorer health outcomes and greater behavior problems. Moderation effects indicated that allostatic load was related to somatic complaints, attention problems, and thought problems only among maltreated children. Risks associated with high waist–hip ratio, low morning cortisol, and high morning dehydroepiandosterone also were related to depressive symptoms only for maltreated children. The results support an allostatic load conceptualization of the impact of high environmental stress and child abuse and neglect on child health and behavioral outcomes and have important implications for long-term physical and mental health.

It has been suggested that biological factors confer increased sensitivity to environmental influences on depressive symptoms during adolescence, a crucial time for the onset of depressive disorders. Given the critical role of the hippocampus in sensitivity to stress and processing of contextual aspects of the environment, investigation of its role in determining sensitivity to environmental context seems warranted. This study prospectively examined hippocampal volume as a measure of sensitivity to the influence of aggressive maternal behavior on change in depressive symptoms from early to midadolescence. The interaction between aggressive maternal behavior and hippocampal volume was found to predict change in depressive symptoms. Significant sex differences also emerged, whereby only for girls were larger bilateral hippocampal volumes more sensitive to the effects of maternal aggressive behavior, particularly with respect to experiencing the protective effects of low levels of maternal aggressiveness. These findings help elucidate the complex relationships between brain structure, environmental factors such as maternal parenting style, and sensitivity to (i.e., risk for, and protection from) the emergence of depression during this life stage. Given that family context risk factors are modifiable, our findings suggest the potential utility of targeted parenting interventions for the prevention and treatment of adolescent depressive disorder.

This randomized controlled trial examined (a) the efficacy of a brief intervention designed to increase the rate of secure infant attachment, (b) the differential susceptibility hypothesis, and (c) whether maternal attachment styles moderated the expected Treatment × Irritability interaction in predicting infant attachment outcomes. Although there was no main effect of treatment, a significant Treatment × Irritability interaction revealed intervention effects for the highly irritable infants only, thus supporting one of two predictions of the differential susceptibility hypothesis: highly irritable infants would have disproportionately better outcomes than moderately irritable infants in better conditions (i.e., with intervention). When separate analyses were conducted with maternal attachment styles, we found significant three-way interactions among treatment, irritability, and each of the examined maternal attachment style dimensions (i.e., secure–fearful and dismissing–preoccupied). Specifically, with more secure mothers, beneficial effects of intervention emerged for highly irritable infants. For more dismissing mothers, the results revealed support for both predictions of the differential susceptibility hypothesis: highly irritable infants, compared to moderately irritable infants, were both more likely to be secure with intervention and less likely to be secure when in the control group. It is interesting that, for more preoccupied mothers, a treatment effect emerged only for moderately irritable infants. We discuss the implications of these findings for the differential susceptibility hypothesis as well as for early intervention.

A substantial amount of research has demonstrated the deleterious effects of chronic stress on memory. However, much less is known about protective factors. In the current study we test the role of maternal responsiveness in buffering the effects of childhood allostatic load on subsequent adolescent working memory. Allostatic load is a marker of cumulative stress on the body that is caused by mobilization of multiple physiological systems in response to chronic environmental demands. Results of the study suggest that allostatic load negatively affects working memory, but that this effect is significantly attenuated in children with responsive mothers.

Within an allostatic load framework, the effect of Gene × Environment (G × E) interactions on diurnal cortisol regulation and internalizing symptomatology were investigated. Variation in the corticotropin releasing hormone receptor 1 (CRHR1) TAT haplotype and serotonin transporter linked polymorphic region (5-HTTLPR) was determined in a sample of maltreated (n = 238, 21.4% with early physical and sexual abuse) and nonmaltreated (n = 255) children (M age = 10.08) participating in a summer research camp. Internalizing and depressive symptoms were assessed by other and self-report. G × E effects for CRHR1 and maltreatment and early abuse on diurnal cortisol regulation were observed; CRHR1 variation was related to cortisol dysregulation only among maltreated children. Early abuse and high internalizing symptoms also interacted to predict atypical diurnal cortisol regulation. The interaction of CRHR1, 5-HTTLPR, and child maltreatment (G × G × E) identified a subgroup of maltreated children with high internalizing symptoms who shared the same combination of the two genes. The findings support an allostatic load perspective on the effects of the chronic stress associated with child maltreatment on cortisol regulation and internalizing symptomatology as moderated by genetic variation.

This article delineates parallel frameworks that grew out of the research on risk and resilience over the past four decades, a framework for research and a framework for practice, and then discusses the promise of an emerging synthesis. The research framework defined the meaning, models, and methods that successfully guided four waves of research to date on the nature and processes involved in human resilience. The applied framework emerged in response to urgent needs of children and families faced by adversity and those charged with helping them, resulting in guidelines for translating the unfolding but incomplete research evidence into action. The application of a resilience approach transformed practice in many fields concerned with promoting resilience in people at risk for problems, revolutionizing the mission, models, measures, and methods of practice to align with the emphasis on positive adaptation and strengths defining a resilience-based approach. Yet these interventions rarely translated back to inform and refine resilience theory in ways that would accelerate progress to promote resilience more effectively. The concluding section on translational synergy discusses the potential for a synthesis of basic and applied resilience frameworks as the next steps toward realizing the original objective and promise of resilience science.