Prenatal diet and childhood atopic dermatitis

The National Institute of Allergy and Infectious Diseases awarded the University of Pennsylvania $100,228 on October 15, 2026, under the Allergy and Infectious Diseases Research program (CFDA 93.855), to conduct a prospective cohort study examining prenatal diet and childhood atopic dermatitis risk.

The project, designated F31AI198148, is the first U.S.-based prospective cohort study investigating the relationship between maternal nutritional exposures during pregnancy and atopic dermatitis onset in children. The research applies the developmental origins of health and disease (DOHAD) framework to examine how prenatal nutritional deficiencies may disrupt fetal immune programming and skin barrier development, pathways implicated in atopic dermatitis pathogenesis. The study responds to rising atopic dermatitis prevalence globally and the condition's substantial disease burden, marked by the highest disability-adjusted life years among all skin diseases.

Work is performed in Philadelphia, Pennsylvania. The period of performance runs through August 31, 2029. The assistance type is a project grant, supporting investigator-initiated research in infectious, immunologic, and allergic diseases at nonprofit research institutions.

Abstract

Despite significant advances in pediatric dermatology, the prevalence of atopic dermatitis (ad) continues to rise-doubling or tripling in industrialized countries and affecting nearly 1 in 4 children worldwide. This chronic inflammatory condition-marked by skin barrier dysfunction and immune dysregulation-causes relentless itching that compels children to scratch until their skin breaks, weeps plasma, and bleeds. Even in the face of these severe symptoms, current treatments offer only brief periods of relief-trapping patients in an unending cycle of flares and remission. The repercussions of this therapeutic limitation extend far beyond discomfort- contributing to a substantial disease burden marked by physical, psychological, and social suffering. This is reflected in ad having the highest disability-adjusted life years (DALYS) among all skin diseases globally. This alarming public health crisis demands urgent investigation into its developmental origins-because only by uncovering them can we identify early-life intervention strategies to prevent disease onset. Numerous studies have already shown that adverse maternal exposures during pregnancy-such as passive smoking, air pollutants, and antibiotics-significantly increase the risk of childhood ad. This evidence of fetal susceptibility points to prenatal diet as the next compelling area of study-given both its potential role in ad development and its highly modifiable nature. The developmental origins of health and disease (DOHAD) framework supports this concept-demonstrating that prenatal nutritional deficiencies can disrupt fetal immune programming and organ development. These disrupted processes align with the known pathogenesis of ad-which is widely attributed to immune dysfunction and compromised skin barrier development. To advance our understanding of this relationship, this F31 proposal introduces the first U.S.-based prospective cohort study examining the impact of prenatal diet on childhood ad. Through the environmental influences on child health outcomes (ECHO) program, this study will analyze 1,673 maternal-child dyads from pregnancy through early childhood-with follow-up beginning at birth and continuing until the development of childhood ad or censoring due to loss to follow-up or the end of follow-up (defined as age 6). Prenatal diet (EXPOSURE) will be assessed using two validated indices-the healthy eating index (HEI) for dietary quality and the empirical dietary inflammatory pattern (EDIP) for inflammatory potential. This study will investigate how prenatal dietary quality (aim 1), dietary inflammatory potential (aim 2), and their joint effects (exploratory aim) influence both the time-to-childhood ad development (primary outcome) and the initial severity at onset (secondary outcome). Ultimately, this F31 proposal aims to identify modifiable prenatal dietary factors to inform future intervention studies and deepen the understanding of early-life determinants of ad.