Exploring joint HPA–inflammatory stress response profiles in adolescent girls: Implications for developmental models of neuroendocrine dysregulation

Abstract

Prior research has struggled to differentiate cortisol stress response patterns reflective of well-regulated versus dysregulated hypothalamic-pituitary-adrenal (HPA) axis function among adolescents. Here, we show how exploring profiles of joint HPAinflammatory stress responsivity, and linking those profiles to pubertal development and peer stress exposure may aid such distinction. Adolescent girls (N = 157, M age = 14.72 years, SD = 1.38) at risk for psychopathology completed assessments of salivary cortisol and pro-inflammatory cytokines (i.e., tumor necrosis factor-α, interleukin-1β, and interleukin-6) prior to and following the Trier Social Stress Test. Adolescents, a close friend, and a caregiver completed questionnaire measures of peer stress and pubertal status. Multitrajectory modeling of adolescents' cortisol and cytokine levels revealed three profiles: low cortisol response-stably low cytokine (n = 75), high cortisol response-stably moderate cytokine (n = 47), and low cortisol response-stably high cytokine (n = 35). Relative to low cortisol response-stably low cytokine, adolescents exhibiting the high cortisol response-stably moderate cytokine profile were more advanced in their pubertal development, but presented with similarly low levels of peer stress exposure. Despite showing cortisol responses that were indistinguishable from low cortisol response-stably low cytokine, adolescents exhibiting the low

Stress system concordance as a predictor of longitudinal patterns of resilience in adolescence

“…Our study contributes to a burgeoning literature highlighting the promise of multiple-levels-of-analysis, person-centered approaches in characterizing risk and resilience processes (Cicchetti & Dawson, 2002; Cicchetti & Rogosch, 1996), with implications for the evaluation of interventions designed to move biological rhythms implicated as resilience mechanisms. For example, awareness of the utility of multi-system approaches (e.g., analyzing HPA function in tandem with peripheral systems) in distinguishing well-regulated versus dysregulated biological function has begun to increase (Bendezú, Calhoun, et al, 2022; Buss et al, 2018; Chen et al, 2020). However, biologically potent interventions have overwhelmingly focused on a single biomarker, notably cortisol (Dozier, Roben, Caron, Hoye, & Bernard, 2018; Fisher et al, 2016).…”

Stakekold ZXSY Brazil, Precision Medicine in Pediatric Clinic: Reward Deficiency Syndrome (RDS) Is Surprisingly Evolving and Found Everywhere: Is It “Blowing in the Wind”? Yes, but how Syndrome Z.

“…Cortisol levels increase in the child when separated from the parents briefly (child stressed by chronic exposures), while endogenous opiates, glutamate, and dopaminergic systems are responsible for the development of emotional regulation capacity [80][81][82][83][84][85].…”

“…. These brain regions work for the initial acquisition and subsequent expression of fear memory [72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87].…”

“…There are numerous studies with evidence of disorders related to ACE + PTSD and lasting effects on the structure and function of neural stress-regulating circuits. Stressful factors such as ACE and PTSD alter the maturation of the hippocampus, amygdala and ACC, causing changes in control and response to stress, emotional dysregulation, which with the increase of glucocorticoids, also occur dendritic atrophy and suppression of neurogenesis, as they have high density and effects of glucocorticoid receptors [72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87].…”

Screening for Neuroprotective and Rapid Antidepressant-like Effects of 20 Essential Oils

“…Dysregulation of the HPA axis and the resulting elevations in corticotrophin-releasing hormone, adrenocorticotropic hormone, and cortisol or corticosterone (CORT) levels have been proposed as key mechanisms underlying the development of depression [7,8]. A dysregulated HPA axis activity is proposed to be accompanied by the overproduction of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, or IL-1β, which leads to the loss of hippocampal neurogenesis and promotion of depression-like behaviors [9,10]. In addition, chronic exposure to glucocorticoids such as cortisol or CORT can lead to dysfunction prefrontal cortex or atrophy of the hippocampus and structural deficits in the dentate gyrus area, which are all brain regions responsible for mood regulation [11,12].…”