Higher Fetal Cortisol Levels Linked to Sleep Onset Delays

INDIANAPOLIS — Higher levels of neonatal hair cortisol, a measure of fetal cortisol production in the third trimester, may have a negative effect on sleep health among infants, according to a longitudinal study.

Among 70 infants in the Care Project study, greater neonatal hair cortisol levels at birth predicted longer sleep onset latency at 7 months (r=0.32, P=0.017), after controlling for gestational age and income-to-needs ratio, reported Melissa Nevarez-Brewster, a graduate student in neurodevelopmental research at the University of Denver, at the annual SLEEP meeting, hosted jointly by the American Academy of Sleep Medicine and the Sleep Research Society.

However, neonatal hair cortisol was not associated with nighttime sleep duration (r = -0.17, P=0.21), nighttime wake duration (r=0.13, P=0.36), or number of night awakenings (r = -0.13, P=0.32).

In an interview with MedPage Today, Nevarez-Brewster said the significance of the preliminary findings remains unknown and more study is needed to understand the effects of neonatal cortisol levels on sleep, if any, later in infancy.

“This study only linked higher neonatal hair cortisol to longer sleep onset latency and not overall sleep at 7 months,” she noted. “We know that sleep health in infancy is related to a lot of other measures of health and well-being later on. But we need to bridge that gap and see if hair cortisol is related to those sleep health outcomes later in life.”

Cortisol is produced in the hypothalamic-pituitary-adrenal (HPA) axis. This system is inhibited during deep sleep, while HPA activation can lead to arousal, fragmented sleep, less overall sleep, and other sleep issues.

HPA axis dysregulation is commonly seen in obesity, sleep deprivation, and sleep disorders such as obstructive sleep apnea and insomnia. Several studies have suggested that higher cortisol levels in adults play a role in some sleep disorders.

In a 2014 study, for example, sleep deprivation was found to be associated with both elevated resting cortisol release and with an exaggerated cortisol response to a stressor indicative of elevated HPA axis responses in healthy adults.

Nevarez-Brewster said the studies in adults led to the newborn study, with the goal of examining whether cortisol in newborns plays a role in regulating sleep during the early postnatal period.

The study included 70 infants with an average gestational age at birth of 39.4 weeks. Girls made up 57.1% of the cohort.

Neonatal hair cortisol samples were collected, on average, 1.7 days after birth, and infant sleep health was assessed at 7 months with the Brief Infant Sleep Questionnaire, a parent-reported sleep assessment tool for infants and toddlers.

Nevarez-Brewster said that late gestational cortisol may “inform the maturation of sleep and the accumulation of sleep pressure throughout the day,” but she added that it is unclear why neonatal hair cortisol was predictive of longer sleep onset latency, and not sleep duration.

The researchers are still collecting sleep data on the children in the study, who are now around 3 years old.

“The next step is really looking to see if the neonatal hair cortisol that we collected shortly after birth is related to sleep health at age 3,” she explained. “Maybe we will only see this at 7 months. Maybe we will still see this association at age 3. Determining this is a critical next step that we are really excited about.”

If the association is confirmed, Nevarez-Brewster said it might be possible to improve infant sleep health with interventions designed to reduce maternal cortisol levels in the last trimester of pregnancy.