# Associations of lifetime stressors and health behaviors with inflammation in young adults previously placed in youth residential care

**Authors:** David Bürgin, Kristen Nishimi, Vera Clemens, Maria Meier, Eva Unternaehrer, Laura Gurri, Evelyne Bruttin, Nicolas Rohleder, Paul Klauser, Daniella Dwir, Nimmy Varghese, Anne Eckert, Süheyla Seker, Delfine d’Huart, Cyril Boonmann, Marc Schmid, Aoife O'Donovan

PMC · DOI: 10.1016/j.bbih.2025.101098 · 2025-09-10

## TL;DR

This study found that health behaviors, not stressors, were linked to inflammation in young adults with high stress exposure.

## Contribution

The study reveals that health behaviors, not stressor exposure, influence inflammation in highly stress-exposed individuals.

## Key findings

- Stressors were not significantly associated with inflammatory markers.
- Risky behaviors increased pro-inflammatory markers and reduced anti-inflammatory markers.
- Protective behaviors were linked to lower pro-inflammatory markers.

## Abstract

Early life stressors (ELS) and stressful life events (SLEs) increase the risk for various physical health conditions, and health behaviors can modulate stress-associated risks. A key mechanism linking both lifetime stress and health behaviors with physical health outcomes is chronic low-grade inflammation. However, it is unclear how both stressor exposure and more proximal health behaviors are associated with inflammation in highly stress-exposed groups.

Here, we investigated associations of lifetime stressors and health behaviors with peripheral inflammation in a highly stress exposed sample of young adults previously placed within youth residential care in Switzerland.

We examined 126 young adults (MAge = 26.3 years; 31 % female) who completed questionnaires to assess ELS, SLEs, and risky and protective health behaviors. Inflammatory markers (C-reactive protein [CRP], interleukin [IL]-6, tumor necrosis factor [TNF]-α, IL-10, and IL-1ra) were measured in venous blood using high sensitivity enzyme-linked immunosorbent assays (hsELISAs). Regressions estimated associations between ELS, SLEs, and health behaviors with each inflammatory marker.

Our sample reported high levels of ELS and SLEs, as well as high levels of risky health behaviors. ELS and SLEs were mostly unassociated with young adult health behaviors, and both ELS and SLEs were not associated with inflammatory markers, adjusting for covariates. Regarding behavior, nicotine dependence was associated with higher pro-inflammatory markers and alcohol abuse marginally with a lower anti-inflammatory marker, while physical activity and better sleep quality were associated with lower pro-inflammatory markers, adjusting for covariates.

Among individuals with high levels of lifetime stress, cumulative ELS and SLEs were unassociated with inflammation, whereas risky behaviors were associated with higher, and protective behaviors with lower inflammatory markers. Interventions that reduce risky and promote protective health behaviors may lower inflammation and promote long-term health among individuals who have experienced high lifetime stressors exposure.

•Stressors were not significantly associated with five inflammatory markers tested in young adults.•Risky behaviors were related to higher pro- and lower anti-inflammatory markers.•Protective behaviors were related to lower pro-inflammatory markers.•Health behaviors were associated with inflammation in a highly stress exposed sample.

Stressors were not significantly associated with five inflammatory markers tested in young adults.

Risky behaviors were related to higher pro- and lower anti-inflammatory markers.

Protective behaviors were related to lower pro-inflammatory markers.

Health behaviors were associated with inflammation in a highly stress exposed sample.

## Linked entities

- **Proteins:** IL6 (interleukin 6), IL10 (interleukin 10)

## Full-text entities

- **Genes:** IL1RN (interleukin 1 receptor antagonist) [NCBI Gene 3557] {aka CRMO2, DIRA, ICIL-1RA, IL-1RN, IL-1ra, IL-1ra3}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** alcohol abuse (MESH:D000437), Inflammatory (MESH:D007249), nicotine dependence (MESH:D014029)

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12629739/full.md

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Source: https://tomesphere.com/paper/PMC12629739