To examine the association between second-trimester maternal serum 25-hydroxyvitamin D concentrations and risk of small for gestational age (SGA) in singleton live births.
We assayed serum samples at 12–26 weeks of gestation for 25-hydroxyvitamin D in a sample of participants in a multicenter clinical trial of low-dose aspirin for the prevention of preeclampsia in high-risk women (n=792). Multivariable log-binomial regression models were used to assess the association between 25-hydroxyvitamin D and risk of SGA (birth weight less than the 10th percentile for gestational age) after adjustment for confounders including maternal prepregnancy obesity, race, treatment allocation, and risk group.
Thirteen percent of neonates were SGA at birth. Mean (standard deviation) 25-hydroxyvitamin D concentrations were lower in women who delivered SGA (57.9 [29.9] nmol/L) compared with non-SGA neonates (64.8 [29.3] nmol/L, P=.028). In adjusted models, 25-hydroxyvitamin D concentrations of 50–74 nmol/L and 75 nmol/L or greater compared with less than 30 nmol/L were associated with 43% (95% confidence interval [CI] 0.33–0.99) and 54% (95% CI 0.24–0.87) reductions in risk of SGA, respectively. Race and maternal obesity each modified this association. White women with 25-hydroxyvitamin D 50 nmol/L or greater compared with less than 50 nmol/L had a 68% reduction in SGA risk (adjusted risk ratio 0.32, 95% CI 0.17–0.63) and nonobese women with 25-hydroxyvitamin D 50 nmol/L or greater compared with less than 50 nmol/L had a 50% reduction in SGA risk (adjusted risk ratio 0.50, 95% CI 0.31–0.82). There was no association between 25-hydroxyvitamin D and risk of SGA in black or obese mothers.
Maternal vitamin D status in the second trimester is associated with risk of SGA among all women and in the subgroups of white and nonobese women.
Second-trimester maternal vitamin D status is associated with risk of small for gestational age at birth among all women and in the subgroups of white and nonobese women.
Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, the Division of Maternal-Fetal Medicine, Magee-Women’s Hospital, and the Departments of Obstetrics, Gynecology and Reproductive Sciences and Pediatrics, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.
Corresponding author: Lisa M. Bodnar, PhD, MPH, RD, University of Pittsburgh Graduate School of Public Health, A742 Crabtree Hall, 130 DeSoto Street, Pittsburgh, PA 15261; e-mail: firstname.lastname@example.org.
Supported by the National Institutes of Health grant HD056999 (Principal Investigator: Dr Bodnar).
The authors thank Mark Klebanoff for his assistance with analysis methods and Jill Diesel and Katharyn Baca for their assistance with data preparation.
Presented as a scientific poster at the Experimental Biology Meeting, April 20–24, 2013, Boston, Massachusetts.
Financial Disclosure The authors did not report any potential conflicts of interest.