Aims
Prenatal alcohol exposure (PAE) increases the risk of adverse pregnancy outcomes including miscarriage, low birthweight, and neurodevelopmental abnormalities, which may be mediated by altered placental development. PAE is associated with alterations to placental vasculature, gene expression, and DNA methylation (DNAm) (1). Choline and folate are dietary micronutrients that serve as methyl donors for DNAm, however their availability may be compromised by alcohol consumption (2). This study investigated the impact of PAE on maternal and placental methyl donors, placental growth and the cerebroplacental ratio (CPR).
Methods
Data and samples were collected from women from the Queensland Family Cohort and classified into PAE (n=302) or abstinent/control (n=109). Maternal diet, placental measurements and Doppler ultrasound measures were examined during the 3rd trimester. Plasma folate was measured using a COBAS analyser. Plasma choline and placental methyl donors were measured by mass spectrometry. Placental gene expression was quantified by qPCR. Placental data were analysed separately by fetal sex.
Results
PAE was reported by 73.5% of participants. Most women (77%) took supplements containing ≥400µg folic acid, while few (27%) met the adequate intake for choline. This was consistent across control and PAE groups. Placental content of folate and choline were not altered by PAE, however, in female placentas, the methyl donor s-adenosylmethionine was increased in the PAE group (P<0.05), as were expression of the choline transporter, CTL1, and placental growth factor (PlGF) (P<0.05). In male placentas, expression of DNA methyltransferases (DNMTs) and (PlGF) were reduced in the PAE group (P<0.05), and placental thickness was decreased (P<0.05). CPR was lower in the PAE group (<0.05), with 11% of male fetuses, but no female fetuses, falling below the normal range, indicative of placental insufficiency.
Conclusion
PAE is associated with sex-specific alterations in the placenta, which may result in male fetuses being more vulnerable to adverse outcomes.