A study published in Nature has uncovered a direct biological link between maternal stress during pregnancy and the development of eczema in newborns, shedding light on a long-suspected connection.
Stress-triggered HPA Fluctuations
More specifically, fluctuations in the maternal hypothalamic–pituitary–adrenal (HPA) axis, triggered by stress, lead to molecular disruptions in the fetus’s neuroimmune system and early-onset eczema in infants.
The study, conducted in mice, showed that offspring of stressed mothers had dysregulated mast cells and skin-projecting neurons. These changes made the newborns highly susceptible to eczema, even from harmless mechanical friction on their skin, per the report.
The source? Elevated levels of corticosterone, a stress hormone, in the amniotic fluid, which altered the programming of fetal mast cells and sensory neurons.
Normalizing Corticosterone Levels
Encouragingly, the researchers also discovered potential solutions. By normalizing maternal corticosterone levels or genetically depleting specific mast cells during pregnancy, they were able to prevent immune dysregulation in the fetus and protect against eczema after birth.
This study introduces a new model for understanding pediatric eczema, suggesting it originates in utero. While the findings presented are in a mouse model, they deepen our understanding of the prenatal origins of eczema and could open the door to potential therapeutic interventions for at-risk pregnancies.
