Amniotic fluid cortisol predicts neonatal and infant development in non-stressed rhesus monkeys: Implications for prenatal stress

Abstract

Prenatal stress adversely affects offspring development, with fetal cortisol (CORT) exposure being a primary hypothesized mechanism for stress-induced developmental deficits. Fetal CORT exposure can be assessed via measurements in amniotic fluid. However, in humans, amniocentesis is typically only performed for clinical reasons such as karyotyping; thus, amniotic fluid CORT cannot be obtained from a random sample. To test the hypothesis that fetal CORT exposure predicts neonatal and infant development in healthy primates, we measured amniotic fluid CORT in N = 18 healthy rhesus macaque (Macaca mulatta) dams (50:50 female:male infants) between 80 and 124 days gestation (mean ± SEM = 98.3 ± 2.9 days out of 165 days gestational length; i.e., second trimester). Maternal hair cortisol concentrations (HCCs) were assessed throughout pregnancy and lactation. Offspring were assessed for physical growth, neurological development, cognitive development, and HCCs across postnatal days 30–180. Controlling for gestational age at amniocentesis, higher amniotic fluid CORT significantly predicted slower infant growth rate (g/day) in the first 30 days (β = −0.19; R² = 0.71, p = .008), poorer sensorimotor scores on the day 30 neonatal assessment (β = −0.28; R² = 0.76, p = .015), and longer time to complete training (β = 0.48; R² = 0.54, p = .026), but better performance (β = 0.91; R² = 0.60, p = .011) on a discrimination cognitive task at 120–180 days. Amniotic fluid CORT was not associated with maternal or infant HCCs. Although these results are correlative, they raise the intriguing possibility that fetal CORT exposure in non-stress-exposed primates, as measured by amniotic fluid CORT, programs multiple aspects of neonatal and infant development. On the other hand, amniotic fluid CORT may not relate to chronic CORT levels in either mothers or infants when assessed by hair sampling.