Circadian rhythms align physiology and behaviour with environmental time-of-day cues (e.g. light/dark cycle) and are vital for normal functioning of organisms. Cells receive circadian inputs via daily fluctuations in hormones (e.g. melatonin and cortisol) and expression of cellular clock genes (e.g. Clock, Bmal1, Per1-3 and Cry1-2). Circadian variation is an intrinsic component of human physiology, developing during late fetal life. Fetal circadian rhythms result predominantly from placentally transmitted maternal circadian cues (e.g. melatonin and cortisol), as the fetus is unable to synthesise these hormones until near term or early postnatal life. Melatonin and cortisol exhibit circadian rhythms in cord blood of newborn babies, hence the maternally derived time-of-day signals in the fetus persist until term. Furthermore, the placenta expresses clock genes and aspects of placental function exhibit circadian rhythmicity
Disruption of maternal circadian rhythmicity can occur through multiple mechanisms e.g shift work during pregnancy and maternal obesity. Importantly, both insults can potentially impact on placental function to decrease fetal growth, which in turn programmes offspring for adult onset diseases including type II diabetes, obesity and hypertension.
Like offspring from mothers with disrupted circadian rhythms, preterm babies are programmed for adult onset diseases. Circadian inputs to the developing fetus are abruptly disrupted by preterm birth due to removal of crucial time-of-day maternal hormonal signals (melatonin/cortisol) and extended admission to the continuously highly illuminated and noisy environment of the neonatal intensive care unit (NICU): continuous light and noise exposure disrupts the development of co-ordinated circadian rhythms. Importantly, reintroduction of light/dark cycles to preterm neonates improves immediate growth trajectories and health, but the long-term benefits are unknown.