Multiple adverse experiences and child cognitive development

The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation (allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions (allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load.

Childhood multiple risk factor exposure exceeds the adverse developmental impacts of singular exposures. Multiple risk factor exposure may also explain why sociodemographic variables (e.g., poverty) can have adverse consequences. Most research on multiple risk factor exposure has relied upon cumulative risk (CR) as the measure of multiple risk. CR is constructed by dichotomizing each risk factor exposure (0 = no risk; 1 = risk) and then summing the dichotomous scores. Despite its widespread use in developmental psychology and elsewhere, CR has several shortcomings: Risk is designated arbitrarily; data on risk intensity are lost; and the index is additive, precluding the possibility of statistical interactions between risk factors. On the other hand, theoretically more compelling multiple risk metrics prove untenable because of low statistical power, extreme higher order interaction terms, low robustness, and collinearity among risk factors. CR multiple risk metrics are parsimonious, are statistically sensitive even with small samples, and make no assumptions about the relative strengths of multiple risk factors or their collinearity. CR also fits well with underlying theoretical models (e.g., Bronfenbrenner's, 1979, bioecological model; McEwen's, 1998, allostasis model of chronic stress; and Ellis, Figueredo, Brumbach, & Schlomer's, 2009, developmental evolutionary theory) concerning why multiple risk factor exposure is more harmful than singular risk exposure. We review the child CR literature, comparing CR to alternative multiple risk measurement models. We also discuss strengths and weaknesses of developmental CR research, offering analytic and theoretical suggestions to strengthen this growing area of scholarship. Finally, we highlight intervention and policy implications of CR and child development research and theory. © 2013 American Psychological Association

Stress begins in the brain and affects the brain, as well as the rest of the body. Acute stress responses promote adaptation and survival via responses of neural, cardiovascular, autonomic, immune and metabolic systems. Chronic stress can promote and exacerbate pathophysiology through the same systems that are dysregulated. The burden of chronic stress and accompanying changes in personal behaviors (smoking, eating too much, drinking, poor quality sleep; otherwise referred to as "lifestyle") is called allostatic overload. Brain regions such as hippocampus, prefrontal cortex and amygdala respond to acute and chronic stress and show changes in morphology and chemistry that are largely reversible if the chronic stress lasts for weeks. However, it is not clear whether prolonged stress for many months or years may have irreversible effects on the brain. The adaptive plasticity of chronic stress involves many mediators, including glucocorticoids, excitatory amino acids, endogenous factors such as brain neurotrophic factor (BDNF), polysialated neural cell adhesion molecule (PSA-NCAM) and tissue plasminogen activator (tPA). The role of this stress-induced remodeling of neural circuitry is discussed in relation to psychiatric illnesses, as well as chronic stress and the concept of top-down regulation of cognitive, autonomic and neuroendocrine function. This concept leads to a different way of regarding more holistic manipulations, such as physical activity and social support as an important complement to pharmaceutical therapy in treatment of the common phenomenon of being "stressed out". Policies of government and the private sector play an important role in this top-down view of minimizing the burden of chronic stress and related lifestyle (i.e. allostatic overload).