Study Links Childhood Adversity to Mitochondrial Changes and Atopic Dermatitis Risk

Key Takeaways

• Greater exposure to adverse childhood experiences (ACEs) was associated with lower mitochondrial DNA copy number (mtDNAcn) in children.
• Lower mtDNAcn was linked to increased odds of atopic dermatitis, but not asthma or allergic rhinitis.
• Authors said the findings suggest mitochondrial dysfunction may represent a biologic pathway connecting childhood stress and atopic disease.

A new study published in Psychoneuroendocrinology suggests that adverse childhood experiences (ACEs) may contribute to biologic changes associated with atopic disease, identifying mitochondrial DNA copy number (mtDNAcn) as a potential mechanistic link between early-life stress and atopic dermatitis.

The investigators conducted a cross-sectional analysis of 226 children enrolled in the Pediatric ACEs Screening and Resiliency Study. Participants were recruited during well-child visits, and caregivers reported ACE exposure as well as physician diagnoses of asthma, atopic dermatitis, and allergic rhinitis. Buccal swab samples were collected to measure mtDNAcn using quantitative polymerase chain reaction.

Mitochondrial Biomarkers May Connect Childhood Stress and Skin Disease

The study population was predominantly non-Hispanic Black and female, with a mean age of 5.6 years. Most caregivers had completed high school.

After multivariable adjustment, greater ACE exposure was associated with lower mtDNAcn. Investigators also found that lower mtDNAcn was associated with increased odds of atopic dermatitis. However, mtDNAcn was not significantly associated with asthma or allergic rhinitis.

The findings build on previous evidence suggesting that chronic activation of the neuroendocrine stress response may alter mitochondrial function. According to the authors, these mitochondrial changes could represent one biologic pathway through which psychosocial stress influences immune-mediated disease in childhood.

Study limitations include its cross-sectional design, which precludes conclusions regarding causality, and reliance on caregiver-reported diagnoses and ACE exposure. The relatively modest sample size may also limit generalizability.

"Our results suggest that greater exposure to ACEs is associated with lower mtDNAcn in children, and that having lower mtDNAcn is associated with greater odds of atopic dermatitis," the authors wrote. "Future work should measure other biomarkers of mitochondrial stress to understand this potential mechanistic relationship between adverse childhood experiences and atopic disease in children."

Source

Díaz LM, Thakur N, Lewis SC, et al. Psychoneuroendocrinology. Published online June 9, 2026. doi:10.1016/j.psyneuen.2026.107936