PubMed · 5460846
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A D Gunn. 1970-01-29. The normal infant.. https://pubmed.ncbi.nlm.nih.gov/5460846/
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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.
A population-based multicentre study, comprising all very low birthweight (VLBW; < or = 1,500 g) infants born alive in the south-east region of Sweden during a 15-month period, was performed in the late 1980s. Among the VLBW infants there were 107 lifebirths (a rate of 0.72%), 86 (80.4%) neonatal survivors and no late deaths. Twenty (18.4%) had intracranial complications, two (2.3%) retinopathy of prematurity, grade 3, and six (5.6%) bronchopulmonary dysplasia. At follow-up at 18 months of uncorrected age, the VLBW infants were still lighter in weight and of shorter stature than control group infants. Of the five (5.8%) of the surviving VLBW infants who had significant neurological disorder at 18 months of age, all had weighed less than 800 g at birth, and had manifested neurological symptoms at 6 months of age. The hospitalisation rate during the first 18 months of life was greater in the VLBW than the control group.