The Neurobiology of Intervention and Prevention in Early Adversity

Abstract

Early adverse experiences are well understood to affect development and well-being, placing individuals at risk for negative physical and mental health outcomes. A growing literature documents the effects of adversity on developing neurobiological systems. Fewer studies have examined stress neurobiology to understand how to mitigate the effects of early adversity. This review summarizes the research on three neurobiological systems relevant to interventions for populations experiencing high levels of early adversity: the hypothalamic-adrenal-pituitary axis, the prefrontal cortex regions involved in executive functioning, and the system involved in threat detection and response, particularly the amygdala. Also discussed is the emerging field of epigenetics and related interventions to mitigate early adversity. Further emphasized is the need for intervention research to integrate knowledge about the neurobiological effects of prenatal stressors (e.g., drug use, alcohol exposure) and early adversity. The review concludes with a discussion of the implications of this research topic for clinical psychology practice and public policy.

Future Directions in the Study of Early-Life Stress and Physical and Emotional Health: Implications of the Neuroimmune Network Hypothesis

“…E. Miller et al, 2011). The burgeoning number of studies that assess HPA or SNS indices in children and adolescents –especially those adopting an experimental/intervention design (Fisher et al, 2016; Slopen, McLaughlin, & Shonkoff, 2014)creates opportunities for the addition of immune measures and assessment of neural activity, which would allow testing of some of the basic tenets of the neuroimmune network model.…”

“…Other researchers have referred to these two dimensions as harmful input (e.g., abuse, trauma) and inadequate input (e.g., neglect/deprivation)(Humphreys & Zeanah, 2014). While many children experience both threat (e.g., physical abuse) and deprivation (e.g., neglect) (Fisher et al, 2016), the fact that threat exposure and deprivation have been linked to differentiable outcomes (e.g., PTSD is more common after threat exposure, whereas attachment disorders are more commonly linked with deprivation, Humphreys & Zeanah, 2014) suggests that this is a viable path forward for early-life stress research aiming to identify the active ingredients of childhood adversity and understand its effects on psychopathology.Much less is known about the differential role of threatening versus depriving experiences in shaping immune outcomes and physical health more broadly. An important future direction in this area would be to empirically examine whether there are distinct neuroimmune signatures related to each of these two dimensions, as well as to explore other potential dimensions of adversity that may be relevant for health (e.g., physical stressors such as exposure to noise and pollutants which are neither threatening per se nor depriving but may interact with psychological stress to amplify allostatic load processes, McEwen & Tucker, 2011).…”

The cortisol awakening response and anterior cingulate cortex function in maltreated depressed versus non-maltreated depressed youth

“…The latter (anticipatory) function of cortisol can be assessed with the cortisol awakening response (CAR). CAR is characterized by a swift rise in cortisol levels shortly after awakening (above already high morning values) followed by a drop in values (Bublitz and Stroud, 2012, 2013; Fisher et al, 2016; Peng et al, 2014) and is regulated by central nervous system (CNS) structures (i.e. hippocampus, anterior cingulate cortex (ACC), pons and mid-brain).…”

“…Examining specific neuroendocrine processes linked to maltreatment status amongst depressed individuals is important given the heterogeneous nature of depressive disorders (Savitz and Drevets, 2009) as well as the enduring CNS and endocrine abnormalities linked to maltreatment (Fisher et al, 2016; Holz et al, 2015). The function of the dACC, a key structure of the PFC, might influence CAR function based on maltreatment history among depressed individuals.…”

Developmental lead and/or prenatal stress exposures followed by different types of behavioral experience result in the divergence of brain epigenetic profiles in a sex, brain region, and time-dependent manner: Implications for neurotoxicology

“…Conversely, early environmental enrichment in mice increased histone acetylation of the BDNF gene in adulthood, but BDNF gene expression levels increased only after stimulation, suggesting that early enrichment permitted rapid increases in BDNF in response to a challenge [50]. Similarly, numerous human studies of traumatic stress during the prenatal period are associated with changes in DNA methylation [44, 51, 52]. …”