Archive for March 5, 2010

Traditionally, it has been evident that some children who show high stress reactivity or inbuilt vulnerability to stress (the diathesis of stress-diathesis model) fare badly when exposed to adverse early life circumstances/events. These adverse environmental influences can range from marital discord in family to stress of being born in a low socio economic status (SES) family or the stress of joining a new peer group.

A new theory however has been gaining ground that these children are orchid children who show high biological and behavioral sensitivity to context and thus can wither in stressful situations while at the same time have the capability to bloom far greater than a normal child given supportive and nurturing environments. One way to conceptualize this is to think of these child as showing greater phenotype variability and adaptability and being more plastic- so the underlying genotype manifest itself differently depending on environmental input. Being more plastic the orchid kids are able to use the environment to their best; or get abused by the environment for the worst.

A new study by Boyce et al looks at the interaction between stressful conditions and stress reactivity in 383 pre-primary children (aged 5-6 years) and reached a similar conclusion that there is indeed an interaction between life stress and stress reactivity such that those who are highly reactive are also more prone to developmental extremes mediated by environmental quality. they thus found that the orchid kids with high stress reactivity showed better adaptation in low life stress conditions, but worse adaptation in high life stress conditions, compared to the dandelions kids who had normal stress reactivity and were more or less immune to life stress. The adaptation measures they measured included clinical and pathological indexes like externalizing symptoms, as well as positive indexes like pro-social behavior, school engagement and academic competence.

The authors looked at two measures of human stress reactivity – Respiratory sinus arrhythmia (RSA)(related to heart rate variability and parasympathetic stress response) and salivary cortisol level changes. High resting RSA/ high RSA reactivity is good and indicates buffering against environmental stress; while low resting RSA / low RSA reactivity is bad and indicates high stress response to stressors . the picture with cortisol reactivity is much unclear and it was not clear (before this study) how cortisol reactivity would interact with life stress to affect adaptation of pre-primary children. the main goal of the study was to find how children stress reactivity and overall family adversity interact to affect adaptation of the child.

Here is the hypothesis in authors own words:

Based on the broad literature on risk and adversity, we hypothesized a robust negative main effect of family adversity across all indices of adaptation. We also expected to find main effects of stress reactivity on adaptation, but given the simultaneous test of interactive effects, as well as the paucity of studies examining the effects of RSA and cortisol reactivity, especially for positive developmental outcomes, and some inconsistencies within such studies, we did not hypothesize the directions of these main effects. More importantly, in accordance with the theory of biological sensitivity to context (Boyce & Ellis, 2005; Ellis et al., 2005), we expected to find evidence that ANS and HPA reactivity moderate the effects of early family adversity on various domains of functioning. We hypothesized that in high-adversity family environments, elevated levels of stress reactivity would be associated with maladaptive outcomes, whereas low stress reactivity would act as a protective factor. In the context of low family adversity, on the other hand, we expected high levels of reactivity to be associated with better adaptation. It is important to note that although biological sensitivity to context should be examined in both positive and negative settings, our assessment focuses on six types of family adversities, and a lack of overall family adversity does not necessarily imply a supportive and nurturing environment. In addition to the hypothesized Adversity × Stress Reactivity interactions, we controlled for children’s sex and tested whether main and interactive effects of adversity and reactivity vary across sex.

And this is what they found too! Here are the results:

The study’s most novel and salient findings emerged when adversity and stress reactivity were considered together, as components of interactions between environmental exposures and measures of biological sensitivity. Stress reactivity moderated the negative effect of family adversity across various domains of adaptation. Overall, the findings are consistent with the stress diathesis hypothesis that high-reactive children show worse adaptive functioning in the context of high adversity. Indeed, such children generally evinced the lowest levels of adaptive functioning of the entire study sample.

However, equally reactive children in settings of low adversity showed the highest levels of adaptation, levels even higher than those of their less reactive counterparts. Specifically, in the context of low family adversity, children who showed high RSA reactivity in response to challenges had the lowest levels of externalizing symptoms and the highest levels of prosocial behaviors and school engagement. Although adaptation showed significant stability from fall to spring, high-reactive children showed improvement in academic competence in the context of low adversity and a decline in competence in the context of high adversity, whereas the inverse was true for low reactive children. Similarly, children who showed high cortisol reactivity to the challenge protocol had the highest levels of prosocial behaviors in the context of low adversity. Further, children exhibiting low RSA reactivity in response to challenges were fully or partially buffered against the harmful effects of adversity on externalizing symptoms, prosocial behavior, and school engagement. Likewise, among children who showed low cortisol reactivity, levels of prosocial behaviors did not significantly change across different levels of adversity.

These findings support the biological sensitivity to context (BSC) theory advanced by Boyce and colleagues (Boyce 2007; Boyce & Ellis, 2005) and the concept of differential susceptibility to environmental influences proposed by Belsky and colleagues (Belsky, 2005; Belsky et al., 2007). This study illustrates that high reactivity is not merely a pathogenic, risk-amplifying response to adversity but can also promote adaptive functioning. Corroborating Boyce and colleagues’ theoretical perspective, children exhibiting high levels of biological sensitivity to context, as indexed by high autonomic and adrenocortical reactivity, were more susceptible to environmental influences in the context of both low and high family adversity. Thus, biologically sensitive children showed the highest levels of symptoms in the context of high family adversity but the highest levels of competence in the context of low family adversity. However, a lack of family adversity does not necessarily imply the presence of a nurturing family environment. Thus, future studies will need to further examine the role of heightened biological sensitivity to context across both stressful, health-undermining and supportive, health-enhancing contexts.

The conceptual figure clearly shows that for low Biological Sensitivity to Context (low BSC) children, adversity has relatively no effect on adaptation/maladaptation. However, for high BSC children, there is an inverse relation between adversity and adaptivity. To me this is further proof of the now robust orchid and dandelion theory of child development.

Obradovi?, J., Bush, N., Stamperdahl, J., Adler, N., & Boyce, W. (2010). Biological Sensitivity to Context: The Interactive Effects of Stress Reactivity and Family Adversity on Socioemotional Behavior and School Readiness Child Development, 81 (1), 270-289 DOI: 10.1111/j.1467-8624.2009.01394.x