UMBILICAL-CORD BETA-ENDORPHIN AND EARLY-CHILDHOOD MOTOR DEVELOPMENT

Stress during delivery has been associated with elevated umbilical cor d 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 previo usly reported. We measured paired maternal and cord plasma beta-endorp hin concentration in a set of 106 low risk deliveries by solid phase t wo-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, regard less of delivery mode, and the two were significantly correlated (r = 0.231; P = 0.017). Multiple regression modeling showed that forceps de livery, maternal beta-endorphin concentration, bradycardia, vaginal de livery, and birth weight each made independent contributions to elevat ed cord beta-endorphin. Depressed cord beta-endorphin predicted more d ay 2 neurological soft signs, lower 6-month mental development, and lo wer 36-month motor score on psychometric tests of the children. Poorer fine motor control and coordination were predominantly associated wit h lower beta-endorphin. Level of cord beta-endorphin independent of de livery stress exerted the primary influence upon child motor developme nt. Higher levels of stress-independent beta-endorphin may play a dire ct role in motor development.