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Associations between Social Adversity and Biomarkers of Inflammation, Stress, and Aging in Children
Matthew S Pantell1,2,3, Patricia P Silveira4,5, Euclides José de Mendonça Filho4,5
1Division of Pediatric Hospital Medicine, Department of Pediatrics, University of California, San Francisco, CA, USA. Matt.Pantell@ucsf.edu.
Insights
Childhood social adversity is linked to higher inflammation and cortisol levels, supporting previous research on stress and health. This large study examined multiple biomarkers in children, finding significant associations with inflammatory markers.
Area of Science:
- Pediatric health
- Biomarkers
- Social determinants of health
Background:
- Childhood social adversity is linked to stress biomarkers, but gaps in knowledge exist.
- Exploration of associations between social adversity and inflammation, neuroendocrine, neuromodulation, and epigenetic aging biomarkers in children.
Purpose of the Study:
- To investigate the relationship between childhood social adversity and various biomarkers.
- To identify specific biomarkers associated with social stress in pediatric populations.
Main Methods:
- Biomarker samples collected from children aged 0-17 years.
- Associations examined with caregiver-reported socioeconomic factors and cumulative adversity.
- Regression analyses and logistic regression used to assess relationships.
Main Results:
- Cumulative social adversity was associated with higher inflammatory markers and cortisol in children.
- A U-shaped distribution was observed for the association between social adversity and these biomarkers.
- No significant relationships found between social adversity and cortisone, neuromodulation biomarkers, or epigenetic aging.
Conclusions:
- Findings support existing research linking social stress to increased inflammation in children.
- This study is among the largest to examine social adversity's impact on pediatric biomarkers, including novel links to cytokine clusters.
Background:
Prior work has found relationships between childhood social adversity and biomarkers of stress, but knowledge gaps remain. To help address these gaps, we explored associations between social adversity and biomarkers of inflammation (interleukin-1β [IL-1β], IL-6, IL-8, tumor necrosis factor-alpha [TNF-α], and salivary cytokine hierarchical "clusters" based on the three interleukins), neuroendocrine function (cortisol, cortisone, dehydroepiandrosterone, testosterone, and progesterone), neuromodulation (N-arachidonoylethanolamine, stearoylethanolamine, oleoylethanolamide, and palmitoylethanolamide), and epigenetic aging (Pediatric-Buccal-Epigenetic clock).
Methods:
We collected biomarker samples of children ages 0-17 recruited from an acute care pediatrics clinic and examined their associations with caregiver-endorsed education, income, social risk factors, and cumulative adversity. We calculated regression-adjusted means for each biomarker and compared associations with social factors using Wald tests. We used logistic regression to predict being in the highest cytokine cluster based on social predictors.
Results:
Our final sample included 537 children but varied based on each biomarker. Cumulative social adversity was significantly associated with having higher levels of all inflammatory markers and with cortisol, displaying a U-shaped distribution. There were no significant relationships between cumulative social adversity and cortisone, neuromodulation biomarkers or epigenetic aging.
Conclusion:
Our findings support prior work suggesting that social stress exposures contribute to increased inflammation in children.
Impact:
Our study is one of the largest studies examining associations between childhood social adversity and biomarkers of inflammation, neuroendocrine function, neuromodulation, and epigenetic aging. It is one of the largest studies to link childhood social adversity to biomarkers of inflammation, and the first of which we are aware to link cumulative social adversity to cytokine clusters. It is also one of the largest studies to examine associations between steroids and epigenetic aging among children, and one of the only studies of which we are aware to examine associations between social adversity and endocannabinoids among children.
Clinical Trial Registration:
NCT02746393.
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