Factors influencing the development of melatonin rhythmicity in humans

• Published in: The journal of clinical endocrinology and metabolism 1996-04, Vol.81 (4), p.1525-1532
• Main Authors: KENNAWAY, D. J, GOBLE, F. C, STAMP, G. E
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Birth Weight; Cesarean Section; Chronobiology; Female; Fetal Growth Retardation - physiopathology; Fetal Growth Retardation - urine; Fetal Membranes, Premature Rupture; Fundamental and applied biological sciences. Psychology; Humans; Infant, Newborn - physiology; Infant, Newborn - urine; Infant, Premature - physiology; Infant, Premature - urine; Male; Melatonin - secretion; Melatonin - urine; Obstetric Labor, Premature; Periodicity; Pre-Eclampsia; Pregnancy; Reference Values; Respiratory Distress Syndrome, Newborn - physiopathology; Respiratory Distress Syndrome, Newborn - urine; Seasons; Twins; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.81.4.1525

The emergence of melatonin rhythmicity was studied in 163 infants between 46-55 weeks postconception by monitoring the excretion of the urinary melatonin metabolite 6-sulfatoxymelatonin (aMT.6S). From this population, we examined the effects of gender, season, multiple birth, home birth, previous sudden infant death syndrome in the family, premature labor, spontaneous rupture of membranes, preeclampsia, intrauterine growth restriction, and nursery lighting on pineal rhythmicity. As previously reported, rhythmic excretion of aMT.6S appeared between 49-55 weeks postconception (9-15 weeks of age) in singleton babies born at term in the hospital. Full-term infants who had a sibling die of sudden infant death syndrome had a pattern of melatonin rhythm development no different from that of the control full-term infants. In contrast, full-term infants born at home and full-term twins born in the hospital had significantly lower aMT.6S excretion than hospital-born singleton infants at the same ages despite similar body weights (e.g. at 52 weeks postconception; 1.8 +/- 0.4, 1.1 +/- 0.3, and 3.6 +/ -0.5 nmol/day, respectively). In full-term infants, there was no difference in the development of melatonin rhythmicity between the sexes, with season or method of delivery (vaginal vs. caesarean). The premature infants were divided into 5 groups (babies born after premature labor, premature rupture of membranes, preeclampsia, intrauterine growth restriction, and fetal distress). All premature infants had a delay in the appearance of aMT.6S rhythms in the urine in relation to chronological age. When the infants were compared on the basis of weeks since conception, those infants born after spontaneous premature labor excreted amounts of aMT.6S no different from those of full-term singleton infants during the period of study. In contrast, the premature rupture of membranes, preeclampsia, and fetal distressed infants excreted 50% less aMT.6S, and intrauterine growth restricted infants excreted 67% less at the same postconceptional ages. These differences were due to reduced nocturnal excretion of the metabolite. In an attempt to accelerate the development of melatonin rhythmicity, premature labor and premature rupture of membranes infants were randomly assigned to be totally deprived of light (using phototherapy eye shields) or partially deprived of light by moving them to a dimly lit room each night for the last 3-8 weeks of their stay in the hospital nursery. Babies born a