Moderate versus severe early life stress: Associations with stress reactivity and regulation in 10–12-year-old children

Abstract

SummaryEarly life stress (ELS) is expected to increase reactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis; however, several recent studies have shown diminished cortisol reactivity among adults and children with ELS exposure. The goal of this study was to examine cortisol activity in 10-12-year-old internationally adopted children to determine if moderate and severe ELS have different impacts on the HPA axis. Salivary cortisol and two measures of autonomic activity were collected in response to the Trier Social Stress Test for Children (TSST-C). Three groups reflecting moderate, severe, and little ELS were studied: early adopted children who came predominantly from foster care overseas (early adopted/foster care (EA/FC), n = 44), later adopted children cared for predominantly in orphanages overseas (late adopted/post-institutionalized (LA/PI), n = 42) and non-adopted (NA) children reared continuously by their middle-to upper-income parents in the United States (n = 38). Diminished cortisol activity was noted for the EA/FC group (moderate ELS), while the LA/PI group (severe ELS) did not differ from the NA group. Overall, few children showed cortisol elevations to the TSST-C in any group. The presence/absence of severe growth delay at adoption proved to be a critical predictive factor in cortisol activity. Regardless of growth delay, however, LA/PI children exhibited higher sympathetic tone than did NA children. These results suggest that moderate ELS is associated with diminished cortisol activity; however, marked individual differences in cortisol activity among the LA/PI children suggest that child factors modify the impact of severe ELS. Lack of effects of severe ELS even for growth delayed children may reflect the restorative effects of adoption or the generally low responsiveness of this age group to the TSST-C. KeywordsCortisol; Group-based trajectory modeling; Growth curve modeling; Linear mixed modeling; Early life stress; Internationally adopted children For over 50 years, animal studies have yielded evidence that early life stress can produce both stress resilience and stress vulnerability (see Levine, 2005). More attention has been paid to the vulnerability findings as these appear to provide a biological explanation for the heighted risk of psychopathology among maltreated children (Felliti et al., 1998;Heim and Nemeroff, 2001;Sanchez et al., 2001;De Bellis, 2005). Nonetheless, there is a large body of animal data showing that early life stress (ELS) can have stress resilience effects, such as reducing fearfulness and neurobiological reactivity to later stressors (see Parker et al., 2006). The distinction between ELS that produces vulnerability and ELS that produces resilience is NIH Public Access Author ManuscriptPsychoneuroendocrinology. Author manuscript; available in PMC 2010 January 1. Published in final edited form as:Psychoneuroendocrinology. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript presumed to lie in individual difference, contextual factors, ...

Causal effects of the early caregiving environment on development of stress response systems in children

“…This pervasive pattern of stress response system hyporesponsivity is inconsistent with patterns observed in the rodent literature following maternal deprivation (1)(2)(3)46) and challenges some prevailing conceptual models of early-life adversity and stress response system development, which argue that adverse environments should lead to elevated physiological reactivity (47,48). The observed pattern of cortisol hyporesponsivity is consistent with several prior studies in humans documenting an association between early-life deprivation and low levels of morning cortisol and blunted cortisol responses to social challenge (20,28,32), although other work has found elevated basal cortisol and heightened cortisol reactivity in children who have experienced social deprivation (17,27). The experimental design of the current study clarifies these inconsistencies in prior observational studies.…”

“…Some studies document hyperreactivity of the SNS and HPA axis following early-life adversity (15)(16)(17)(18)(19) and others observe blunted HPA axis reactivity (20)(21)(22) or discordance between SNS and HPA axis responses (23). Reconciling these inconsistencies has proved challenging for several reasons.…”

“…Reconciling these inconsistencies has proved challenging for several reasons. First, there is considerable heterogeneity in the type, frequency, severity, and cooccurrence of early-life adversities in human studies, including both abuse and neglect (15,18,19,21,22), poverty (24-26), institutional rearing followed by international adoption (17,20,27,28), or accumulation of multiple adversities, ranging from marital conflict to parental psychopathology (29)(30)(31). These exposures not only differ widely from each other, they also vary in their resemblance to the exposure used in animal studies: maternal deprivation.…”

“…These exposures not only differ widely from each other, they also vary in their resemblance to the exposure used in animal studies: maternal deprivation. Lower morning cortisol and blunted cortisol reactivity are the most commonly reported patterns in studies of maternal deprivation related to neglect or institutional rearing following by international adoption (20,28,32), although elevated basal cortisol and cortisol reactivity have also been observed (17,27). Second, existing human research has been unable to identify causal effects of the rearing environment on stress response system development.…”

Interpersonal early‐life trauma alters amygdala connectivity and sustained attention performance

“…It is important to underscore the personal nature of these traumatic events, since they have been documented to lead to more severe symptoms than impersonal traumas like accidents or natural disasters (Perry et al., 1995). Studies of interpersonal early life trauma (I‐ELT) have further revealed increases in reactivity to fear‐conditioning and startle paradigms (Jovanovic et al., 2009, 2011; Ornitz & Pynoos, 1989), decreases in stress regulation (Gunnar, Frenn, Wewerka, & Van Ryzin, 2009), and impaired emotion regulation abilities (McLaughlin, Hatzenbuehler, Mennin, & Nolen‐Hoeksema, 2011). Such behavioral alterations have been associated with increased risk of developing psychopathology in adulthood (Heim & Nemeroff, 2001), especially posttraumatic stress disorder (PTSD) (Lanius, Frewen, Vermetten, & Yehuda, 2010; McKeever & Huff, 2003; Pratchett & Yehuda, 2011).…”