Attenuation of cortisol across development for victims of sexual abuse

Abstract

Inconsistencies exist in literature examining hypothalamic–pituitary–adrenal (HPA) axis activity in children and adults who have experienced childhood abuse. Hence, the extent and manner to which childhood abuse may disrupt HPA axis development is largely unknown. To address these inconsistencies, the developmental course of nonstress cortisol in a long-term longitudinal study was assessed at six time points from childhood through adolescence and into young adulthood to determine whether childhood abuse results in disrupted cortisol activity. Nonstress, morning cortisol was measured in 84 females with confirmed familial sexual abuse and 89 nonabused, comparison females. Although dynamically controlling for co-occurring depression and anxiety, hierarchical linear modeling (HLM) showed that relative to comparison females, the linear trend for abused females was significantly less steep when cortisol was examined across development from age 6 to age 30, t (1, 180)= −22.55, p < .01, indicating attenuation in cortisol activity starting in adolescence with significantly lower levels of cortisol by early adulthood, F (1, 162) =4.78, p < .01. As a more direct test of the attenuation hypothesis, supplemental HLM analyses of data arrayed by time since the disclosure of abuse indicated that cortisol activity was initially significantly higher, t (1, 425) = 2.18, p < .05, and slopes were significantly less steep t (1, 205) = −22.66, p < .01, for abused females. These findings demonstrate how the experience of childhood abuse might disrupt the neurobiology of stress, providing some support for the attenuation hypothesis that victims of abuse may experience cortisol hyposecretion subsequent to a period of heightened secretion.

HPA axis dysregulation in adult adoptees twenty years after severe institutional deprivation in childhood

“…In light of the evidence of decreased cortisol activity and reactivity in adults and children with experience of early adversity (Carpenter et al, 2007;Elzinga et al, 2008;Lovallo et al, 2011;Miller et al, 2007;Power et al, 2012;Schwaiger et al, 2016), it has been proposed that sustained periods of chronic stress, such as psychosocial deprivation and neglect, are initially associated with high levels of circulating cortisol, followed by counter-regulation which eventually results in decreased HPA axis re-/ activity. This attenuation hypothesis (Trickett et al, 2010) is supported by a meta-analysis showing that the more time that had elapsed since trauma emerged, the lower a person's cortisol levels (Miller et al, 2007). Epigenetic alterations have been proposed as a mechanism for the stability of the long-term effects of early environmental influences in general (Mill and Heijmans, 2013) and the long-term setting of the HPA axis in particular (Chen et al, 2012;Murgatroyd et al, 2009;Turecki and Meaney, 2016;Weaver et al, 2004;Zhang and Meaney, 2010).…”

Consecuencias del abuso sexual infantil: una revisión de las variables intervinientes

“…Pero durante esta etapa pueden aparecer también una serie de problemas nuevos. Los problemas externalizantes (p.e., agresiones y problemas conductuales), trastornos disociativos, problemas en las relaciones con los iguales, bajo rendimiento escolar y desregulaciones en los niveles de cortisol y otros trastornos psicobiológi-cos debidos a una desregulación del eje hipotalámico-hipofisario-adrenal (lo que podría explicar los problemas emocionales de las víctimas) son más frecuentes entre niños víctimas de abuso sexual que entre niños no víctimas (Trickett et al, 2001;Trickett, Noll, Susman, Shenk y Putnam, 2010).…”

The STRIVE-ONR Project: Stress Resistance in Virtual Environments

“…The impact of stress on the brain is mediated by the activation of the hypothalamicpituitary-adrenal (HPA) axis, which consists of the stimulation of the paraventricular nucleus of the hypothalamus, resulting in the production of corticotropin releasing hormone (CRH) (Trickett, Noll, Susman, Shenk, & Putnam, 2010). This triggers the pituitary gland to release adrenocorticotropic hormone (ACTH) into the bloodstream.…”