Bibian van der Voorn

63 MATERNAL STRESS REFLECTED IN NEONATAL HAIR GC LEVELS cortisol to inert cortisone by placental 11βHSD2, amniotic fluid cortisone was higher than cortisol 31 . In addition, evidence from studies in adults suggests that hair GCs reflect the body’s HPA axis activity, with hair GCs being associated with long-term integrated salivary cortisol 16 . Thus, neonatal hair GCs plausibly reflect a combination of exposure to maternal GCs, placental CRH, and fetal adrenal maturation. Exposure to excessive pre- and perinatal distress has been associated with permanent impairments in offspring’s neurocognitive development 3-5 . Although the mechanisms behind these associations are not fully elucidated yet, there is some evidence suggesting that disturbances in maternal HPA axis activity during pregnancy could partly explain these effects 9,32 . Therefore, long-term follow-up of our cohort is warranted to explore effects on various aspects of HPA axis development, including stress reactivity and establishment of a diurnal rhythm, aswell as neurodevelopmental and cardiometabolic outcome 10 . The major strength of this study is the unique sample with a wide range of pre- and postnatally experienced stress levels, including an overrepresentation of severely stressed mother-infant pairs. In addition, to the best of our knowledge, this is the first translational study that measured hair GC levels in both mothers and infants who experienced a reliably quantified amount of distress during pregnancy 33 . A limitation of our study is that prenatal HADS-scores were only known for the subgroup of mothers who sought consultation at the POP clinic during their pregnancies. Although the strength of our population was the overrepresentation of severely stressed subjects, their vulnerability made us choose for non-invasive measures of HPA axis activity. Ideally, various aspects of HPA axis activity, such as reactivity and rhythmicity, should have been included too 34 . Moreover, this study was not designed to assess the influence of SAD use. Nonetheless, our data strongly suggested that elevated maternal stress-scores explained the associations between SAD use and maternal hair GCs. In conclusion, we found that pre- and perinatal exposure to excessive maternal stress was associated with a decrease in neonatal hair GC levels, with the largest decrease seen in children of mothers with persistent stress throughout pregnancy. In addition, elevated maternal stress-scores around birth were associated with increased maternal hair GC levels, while elevated stress-scores earlier in gestation had no effect on maternal hair GCs. Accordingly, maternal stress during pregnancy might have increased intra-uterine GC exposure, thereby suppressing fetal HPA axis activity.