Maternal Vitamin D Has Impact on Kids’ Atopic Dermatitis – MD Magazine
A lower intake of Vitamin D in early childhood was also found to be marginally associated with higher persistence of AD though mid-childhood.
Maria Blomberg, Ph.D., research fellow at the Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Car Institute and colleagues reported their findings July 29 at the American Academy of Dermatology Summer Meeting in Boston.
“Vitamin D affects skin barrier and immune function, potentially altering the risk of atopic dermatitis,” the investigators explained, “however, studies relating vitamin D intake and plasma 25(OH)D levels to AD are conflicting.”
The findings emerged from data of Project Viva, a longitudinal research study at Harvard Medical School funded primarily by the National Institutes of Health (NIH) and the U.S. Centers for Disease Control and Prevention.
The current analysis was conducted with 1,418 mother-child pairs, from the Project Viva study population of 2,128 mothers who delivered children from 1999 to 2002.
The associations with prenatal 25(OH)D levels and vitamin D intake, expressed as adjusted odds ratio (aOR), were determined with multivariable logistic regression adjusted for maternal education, parental atopy, child sex, race gestation length and fetal growth, as well as the season for the second trimester blood level determinations, with the inherent possible variation of sunlight exposure.
Atopic dermatitis developed in 35 percent (497/1418) in early childhood, and 15 percent of those included in follow-up had persistent AD (58/389).
The odds of AD in early childhood were reduced if the maternal 25(OH)D level was above 25 nmol/L (aOR= 0.36 with 95 percent Confidence Interval [CI] 0.18-0.72).
Maternal vitamin D intake during pregnancy, however, was not related to the development of AD in the child. A higher intake of vitamin D in early childhood was associated with lower odds of persistent AD in mid-childhood (aOR= 0.73 per 100IU, 95 percent CI 0.54-0.99).
The investigators note that the study limitations included having few childhood 25(OH)D blood samples, no information on sun exposure, and that the occurrence of AD was based on maternal reporting of the child receiving that diagnosis.