Prenatal Maternal Distress Affects Atopic Dermatitis in Offspring Mediated by Oxidative Stress
Chang HY, Suh DI, Yang SI, et al J Allergy Clin Immunol. 2016;138:468-475
The Study
The Cohort for Childhood Origin of Asthma and Allergic Diseases (COCOA) study[1] investigated an inner-city population to assess which factors might influence pediatric allergic disease, including genetics, perinatal environment, maternal lifestyle, and psychosocial stress of both mother and child. The study, conducted in Korea, was longitudinal, prospective, and observational.
Perinatal indoor and outdoor factors (allergens, smoking, pollutants) were measured along with maternal prenatal psychosocial stress and the child's neurodevelopment, perinatal nutrition, and microbiome.
The allergic diseases of interest included asthma, food allergy, rhinoconjunctivitis, and atopic dermatitis (AD). Researchers assessed maternal, paternal, cord, and child blood draws. Through maternal questionnaire responses, they documented stress levels and AD diagnoses. Objective markers of stress were also measured, including placental levels of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) and the antioxidant glutathione.
The researchers concluded that prenatal maternal distress puts offspring at greater risk for AD and that the condition was mediated by oxidative stress.[2] Both depression and anxiety in the mother increased the risk for AD in children. High scores in these areas were also associated with markers of prenatal distress (11β-HSD2) and total glutathione levels.
The authors admit to multiple limitations of the study, including that prenatal distress was measured by survey rather than interview, that one third of study participants were excluded due to missing data, that distress was measured retrospectively, and that the diagnosis of AD relied upon parental report.
