Childbirth-related posttraumatic stress symptoms - examining associations with hair endocannabinoid concentrations during pregnancy and lifetime trauma.

Evidence has linked alterations of the endocannabinoid system with trauma exposure and posttraumatic stress disorder (PTSD). Childbirth-related PTSD symptoms (CB-PTSS) affect about every eighth woman and can negatively influence the entire family. While aetiological models of CB-PTSD include psychological risk factors such as maternal trauma history and negative subjective birth experience (SBE), they lack biological risk indicators. We investigated whether lifetime trauma and CB-PTSS were associated with long-term endocannabinoid concentrations during pregnancy. Further, we tested endocannabinoids as mediators between lifetime trauma and CB-PTSS and whether SBE moderated such mediational paths. Within the prospective cohort study DREAMHAIR, 263 expectant mothers completed trauma assessments and provided hair samples for quantification of long-term endocannabinoid levels (anandamide [AEA], 2-arachidonoylglycerol [1-AG/2-AG], and N-acyl-ethanolamides [NAE]) prior to their anticipated birth date. Two months postpartum, CB-PTSS and SBE were measured. Regression models controlling for relevant confounders showed no association between lifetime trauma and hair endocannabinoids during pregnancy, yet higher number of lifetime trauma events and lower hair AEA were significantly associated with CB-PTSS, with the latter finding not remaining significant when Bonferroni corrections due to multiple testing were applied. While hair AEA did not mediate the association between lifetime trauma and CB-PTSS, the effect of lower hair AEA on CB-PTSS was stronger upon negative SBE. Results suggest greater lifetime trauma and reduced maternal hair AEA during pregnancy may be associated with increased risk for CB-PTSS, particularly upon negative SBE. Findings confirm lifetime trauma as a CB-PTSS risk factor and add important preliminary insights on the role of endocannabinoid ligand alterations and SBE in CB-PTSS pathology.

The association between maternal symptoms of depression and hair glucocorticoids in infants across the perinatal period.

BACKGROUND: Maternal symptoms of depression constitute an early adversity for infants that is considered to exert its effects via the maternal-placental-fetal neuroendocrine axis. Previous research implicates associations between maternal prenatal symptoms of depression and infants' glucocorticoid (GC) levels shortly after birth. To date, associations have not been investigated in the early postnatal period. The current study aimed to investigate the influence of maternal perinatal symptoms of depression on infants' neonatal and postnatal hair GCs providing a retrospective reflection of integrated cortisol secretion in the intrauterine and early postnatal period, respectively. METHODS: As part of a prospective cohort study, hair samples of infants were taken up to two weeks after delivery (N = 152) and again eight weeks after delivery (N = 165). Liquid chromatography-tandem mass spectrometry was used to determine hair cortisol and cortisone in scalp-near 2-cm hair segments. Maternal symptoms of depression were assessed during pregnancy and eight weeks postnatally based on the Edinburgh Postnatal Depression Scale. RESULTS: Higher maternal prenatal symptoms of depression showed a significant association with higher infants' neonatal hair cortisol, when controlling for confounding variables (i.e., gestational age, mode of delivery, parity, storage time, pregnancy complications). A non-significant trend for this effect was found for the hair cortisol-to-cortisone ratio while no effect occurred for hair cortisone. No association of maternal postnatal symptoms of depression with infants' postnatal hair GCs was observed. Further exploratory analyses revealed no relationship between a change of maternal prenatal to postnatal symptoms of depression with the change from infants' neonatal to postnatal hair GC levels or postnatal hair GCs. CONCLUSION: Our results suggest that maternal prenatal symptoms of depression are associated with dysregulated infants' hair cortisol levels mainly incorporated in the intrauterine period which, in turn, might contribute to increased susceptibility for later diseases. However, no relationship was observed in infants' hair samples additionally reflecting hair GCs of the early postnatal period. Future studies should consider research on associations between maternal symptoms of depression and infants' hair GCs also later in life and take into account additional risk factors with potential impacts on GC secretion during early infancy.