Biological sensitivity to context as a dyadic construct: An investigation of child–parent RSA synchrony among low-SES youth

Parenting behaviors are significantly linked to youths’ behavioral adjustment, an association that is moderated by youths’ and parents’ self-regulation. The biological sensitivity to context theory suggests that respiratory sinus arrhythmia (RSA) indexes youths’ varying susceptibility to rearing contexts. However, self-regulation in the family context is increasingly viewed as a process of “coregulation” that is biologically embedded and involves dynamic Parent×Child interactions. No research thus far has examined physiological synchrony as a dyadic biological context that may moderate associations between parenting behaviors and preadolescent adjustment. Using a two-wave sample of 101 low-socioeconomic status (SES) families (children and caretakers; mean age 10.28 years), we employed multilevel modeling to examine dyadic coregulation during a conflict task, indicated by RSA synchrony, as a moderator of the linkages between observed parenting behaviors and preadolescents’ internalizing and externalizing problems. Results showed that high dyadic RSA synchrony resulted in a multiplicative association between parenting and youth adjustment. High dyadic synchrony intensified the relations between parenting behaviors and youth behavior problems, such that in the context of high dyadic synchrony, positive and negative parenting behaviors were associated with decreased and increased behavioral problems, respectively. Parent–child dyadic RSA synchrony is discussed as a potential biomarker of biological sensitivity in youth.

Biological sensitivity to context: A test of the hypothesized U-shaped relation between early adversity and stress responsivity

We conducted signal detection analyses to test for curvilinear, U-shaped relations between early experiences of adversity and heightened physiological responses to challenge, as proposed by biological sensitivity to context theory. Based on analysis of an ethnically diverse sample of 338 kindergarten children (4–6 years old) and their families, we identified levels and types of adversity that, singly and interactively, predicted high (top 25%) and low (bottom 25%) rates of stress reactivity. The results offered support for the hypothesized U-shaped curve and conceptually replicated and extended the work of Ellis, Essex, and Boyce (2005). Across both sympathetic and adrenocortical systems, a disproportionate number of children growing up under conditions characterized by either low or high adversity (as indexed by restrictive parenting, family stress, and family economic condition) displayed heightened stress reactivity, compared with peers growing up under conditions of moderate adversity. Finally, as hypothesized by the adaptive calibration model, a disproportionate number of children who experienced exceptionally stressful family conditions displayed blunted cortisol reactivity to stress.

Biological Sensitivity to Context

It is now well established that early experiences of adversity play a central role in development of many mental health problems in adulthood. However, the effects are more pronounced and detrimental for some individuals compared to others. Informed by the biological sensitivity to context model, an evolutionary-developmental model of individual differences in stress responsivity, the present chapter highlights the role of stress response system as one moderating mechanism in the pathway between early life experiences and development of internalizing and externalizing behaviors. The model posits that the magnitude and integrated patterns of autonomic and adrenocortical responses to psychosocial challenges are indicators of the organisms’ level of susceptibility to both positive and negative environmental influences. The final part of the chapter focuses on the role of early life experiences in programming the functioning of stress response systems, development of adaptive stress responsivity patterns, and related behavioral profiles.

Incorporating epigenetic mechanisms to advance fetal programming theories

Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match–mismatch model (an evolutionary–developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field.

Effects of family cohesion and heart rate reactivity on aggressive/rule-breaking behavior and prosocial behavior in adolescence: The Tracking Adolescents' Individual Lives Survey study

The biological sensitivity to context hypothesis posits that high physiological reactivity (i.e., increases in arousal from baseline) constitutes heightened sensitivity to environmental influences, for better or worse. To test this hypothesis, we examined the interactive effects of family cohesion and heart rate reactivity to a public speaking task on aggressive/rule-breaking and prosocial behavior in a large sample of adolescents (N = 679; M age = 16.14). Multivariate analyses revealed small- to medium-sized main effects of lower family cohesion and lower heart rate reactivity on higher levels of aggressive/rule-breaking and lower levels of prosocial behavior. Although there was some evidence of three-way interactions among family cohesion, heart rate reactivity, and sex in predicting these outcome variables, these interactions were not in the direction predicted by the biological sensitivity to context hypothesis. Instead, heightened reactivity appeared to operate as a protective factor against family adversity, rather than as a susceptibility factor. The results of the present study raise the possibility that stress reactivity may no longer operate as a mechanism of differential susceptibility in adolescence.