Fetal growth restriction is a major risk factor for illness in the neonatal period and throughout life, with the smallest 7.5 percent of infants accounting for two-thirds of infant deaths. Term, low birth weight infants are at least five times more likely to die in the first year and are second only to premature infants in their rates of illness and death. Low birth weight newborns have an increased risk of several adverse outcomes in childhood, including cerebral palsy and hypertension. As adults, low birth weight individuals are at elevated risk for pregnancy-induced hypertension, gestational diabetes, essential hypertension, type 2 diabetes, and cardiovascular disease. The ability both to predict and to treat fetal growth restriction early in gestation has enormous potential to reduce childhood death and suffering.

Some of the most important growth factors during fetal development (i.e., insulin, insulin-like growth factor 2 undergo imprinting, meaning that the copy of the gene inherited from either the mother or father is shut off in most fetal tissues and in the placenta. As part of a large study of child development from pregnancy to age 3, Dr. Ronald Adkins is examining variation in imprinted genes in 500 pairs of mothers and newborn to identify variants in imprinted genes that lead to fetal growth restriction. Recently, Dr. Adkins found variants in the insulin gene that significantly increase the risk of fetal growth restriction and decrease insulin-like growth factor 2 levels in the fetus when inherited from the father, but not the mother. These results are exciting because mouse studies prove that the dietary intake of nutrients such as folate and B12 can influence the expression of imprinted genes. Dr. Adkins plans to follow up his genetic work by determining if the effect that imprinted genes have on fetal growth restriction can be moderated by dietary intervention.