Blunted endocrine response to a combined physical-cognitive stressor in adults with early life adversity

Hengesch, Xenia; Elwenspoek, Martha M C; Schaan, Violetta; Larra, Mauro F.; Finke, Johannes B.; Zhang, Xinwei; Bachmann, Petra; Turner, Jonathan D.; Vögele, Claus; Schächinger, Hartmut

doi:10.1016/j.chiabu.2018.04.002

Cited by 31 publications

(56 citation statements)

References 43 publications

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“…As expected, our ELA participants had low scores of childhood maltreatment (CTQ). However, as we have previously, reported they have a very clear ELA-associated immunophenotype ) and a clear stress-induced HPA axis hyporeactivity (Hengesch et al, 2018), confirming long-term physiological consequences from their exposure to a significant ELA. As we have previously suggested, in the specific case of institutionalization/ adoption, a low CTQ score does not indicate an absence of ELA .…”

Section: Discussionsupporting

confidence: 85%

“…As anticipated, this cohort had an inhibited HPA axis reactivity with a lower corticosterone response to a laboratory stressor, although cardiovascular stress responsiveness was not affected by ELA (Hengesch et al, 2018). This separation is most probably explained by ELA's selectively enhancing central feedbacksensitivity to GC, while the cardiovascular/ autonomic stress reactivity was preserved (Hengesch et al, 2018). Our studies of the EpiPath cohort were the first to report on a broad range of immune markers covering the innate, humoral, and adaptive immune system following ELA.…”

supporting

confidence: 66%

“…This study is based on our EpiPath cohort that consists of young adults who experienced ELA in the form of separation from their parents and/or institutionalization followed by adoption in early childhood and controls reared by their biological parents. As anticipated, this cohort had an inhibited HPA axis reactivity with a lower corticosterone response to a laboratory stressor, although cardiovascular stress responsiveness was not affected by ELA (Hengesch et al, 2018). This separation is most probably explained by ELA's selectively enhancing central feedbacksensitivity to GC, while the cardiovascular/ autonomic stress reactivity was preserved (Hengesch et al, 2018).…”

supporting

confidence: 60%

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Glucocorticoid receptor signaling in leukocytes after early life adversity

et al. 2019

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Early life adversity (ELA) has been associated with inflammation and immunosenescence, as well as hyporeactivity of the HPA axis. Because the immune system and the HPA axis are tightly intertwined around the glucocorticoid receptor (GR), we examined peripheral GR functionality in the EpiPath cohort among participants who either had been exposed to ELA (separation from parents and/or institutionalization followed by adoption; n = 40) or had been reared by their biological parents (n = 72). Expression of the strict GR target genes FKBP5 and GILZ as well as total and 1F and 1H GR transcripts were similar between groups. Furthermore, there were no differences in GR sensitivity, examined by the effects of dexamethasone on IL6 production in LPS-stimulated whole blood. Although we did not find differences in methylation at the GR 1F exon or promoter region, we identified a region of the GR 1H promoter (CpG 1-9) that showed lower methylation levels in ELA. Our results suggest that peripheral GR signaling was unperturbed in our cohort and the observed immune phenotype does not appear to be secondary to an altered GR response to the perturbed HPA axis and glucocorticoid (GC) profile, although we are limited in our measures of GR activity and time points.

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Section: Discussionsupporting

confidence: 85%

supporting

confidence: 66%

supporting

confidence: 60%

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Glucocorticoid receptor signaling in leukocytes after early life adversity

et al. 2019

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“…Mothers who recalled receiving more support for autonomy from caregivers during early childhood tended to display lower SNS arousal (i.e., longer PEP) at rest. Research generally supports a link between SNS activity and early adversity (Ali & Pruessner, 2012;Esposito et al, 2016;Gunnar et al, 2009;Hengesch et al, 2018), however, current understanding of how more normative variations in early experience may shape in-the-moment SNS activation is relatively limited. Our findings here are consistent with evidence of SNS hyperactivity among those exposed to poor early caregiving in childhood and into adulthood (Ali & Pruessner, 2012;Dube et al, 2009;Miller et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Recollections of positive early caregiving relate to sympathetic nervous system activation and chronic inflammation in subsequent generations

Lyons

Wells

Scholtes

et al. 2018

Developmental Psychobiology

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To understand links between early experience and biomarkers of peripheral physiology in adulthood, this study examined associations between quality of early caregiving and markers of sympathetic activation and chronic inflammation in a sample of 52 low‐income mothers and their preschool‐aged children. Mothers reported on levels of positive caregiving experienced during childhood using the Structural Analysis of Social Behavior‐Intrex. Mother and child sympathetic activation was indexed via pre‐ejection period (PEP) at rest, during a dyadic social engagement task, and for children, while interacting with an unfamiliar adult. C‐reactive protein (CRP) was collected using whole blood spots to assess levels of low‐grade chronic inflammation. Results showed that mothers who reported experiencing more warm guidance and support for autonomy in early childhood displayed lower resting sympathetic nervous system activation (i.e., longer PEP) and lower chronic inflammation (i.e., CRP levels). Further, lower maternal chronic inflammation levels were associated with lower sympathetic activation (i.e., longer PEP) in their children at rest, and during social interactions with mother and a female stranger.

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“…There is now a growing literature on the effects of early-life psychosocial adversity on the immune system. We have previously reported the immunophenotype of young adults that had experienced ELA as institutionalization after separation from their parents and subsequently adopted in early childhood compared to those reared by their biological parents (EpiPath cohort) [25]. In this cohort, we surveyed the innate, humoral, and adaptive immune system.…”

Section: Early Life Psychosocial Stressmentioning

confidence: 99%

The COVID-19 Pandemic: Does Our Early Life Environment, Life Trajectory and Socioeconomic Status Determine Disease Susceptibility and Severity?

Holuka

Merz

Fernandes

et al. 2020

IJMS

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A poor socioeconomic environment and social adversity are fundamental determinants of human life span, well-being and health. Previous influenza pandemics showed that socioeconomic factors may determine both disease detection rates and overall outcomes, and preliminary data from the ongoing coronavirus disease (COVID-19) pandemic suggests that this is still true. Over the past years it has become clear that early-life adversity (ELA) plays a critical role biasing the immune system towards a pro-inflammatory and senescent phenotype many years later. Cytotoxic T-lymphocytes (CTL) appear to be particularly sensitive to the early life social environment. As we understand more about the immune response to SARS-CoV-2 it appears that a functional CTL (CD8+) response is required to clear the infection and COVID-19 severity is increased as the CD8+ response becomes somehow diminished or exhausted. This raises the hypothesis that the ELA-induced pro-inflammatory and senescent phenotype may play a role in determining the clinical course of COVID-19, and the convergence of ELA-induced senescence and COVID-19 induced exhaustion represents the worst-case scenario with the least effective T-cell response. If the correct data is collected, it may be possible to separate the early life elements that have made people particularly vulnerable to COVID-19 many years later. This will, naturally, then help us identify those that are most at risk from developing the severest forms of COVID-19. In order to do this, we need to recognize socioeconomic and early-life factors as genuine medically and clinically relevant data that urgently need to be collected. Finally, many biological samples have been collected in the ongoing studies. The mechanisms linking the early life environment with a defined later-life phenotype are starting to be elucidated, and perhaps hold the key to understanding inequalities and differences in the severity of COVID-19.

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Blunted endocrine response to a combined physical-cognitive stressor in adults with early life adversity

Cited by 31 publications

References 43 publications

Glucocorticoid receptor signaling in leukocytes after early life adversity

Glucocorticoid receptor signaling in leukocytes after early life adversity

Recollections of positive early caregiving relate to sympathetic nervous system activation and chronic inflammation in subsequent generations

The COVID-19 Pandemic: Does Our Early Life Environment, Life Trajectory and Socioeconomic Status Determine Disease Susceptibility and Severity?

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