Stress during delivery has been associated with elevated umbilical cord plasma beta-endorphin levels. Published research suggests that much cord beta-endorphin originates from fetal pituitary. Intact pituitary function is required for normal growth and development. Relationships between cord beta-endorphin and child development have not been previously reported. We measured paired maternal and cord plasma beta-endorphin concentration in a set of 106 low risk deliveries by solid phase two-site immunoradiometric assay. Geometric mean maternal and cord beta-endorphin concentrations were 128 pg/ml and 196 pg/ml, respectively, with corresponding ranges of 33-533 pg/ml and 70-579 pg/ml. Cord beta-endorphin concentration was significantly higher than maternal, regardless of delivery mode, and the two were significantly correlated (r = 0.231; P = 0.017). Multiple regression modeling showed that forceps delivery, maternal beta-endorphin concentration, bradycardia, vaginal delivery, and birth weight each made independent contributions to elevated cord beta-endorphin. Depressed cord beta-endorphin predicted more day 2 neurological soft signs, lower 6-month mental development, and lower 36-month motor score on psychometric tests of the children. Poorer fine motor control and coordination were predominantly associated with lower beta-endorphin. Level of cord beta-endorphin independent of delivery stress exerted the primary influence upon child motor development. Higher levels of stress-independent beta-endorphin may play a direct role in motor development.