Alcohol Consumption and Smoking During Pregnancy Alters Maternal Plasma Fatty Acid Composition: Association with Fetal Alcohol Spectrum Disorders (P11-028-19)

Abstract

ObjectivesPolyunsaturated fatty acids (PUFA) are vital for optimal fetal neuronal development. This study examined the relationship between maternal alcohol consumption and smoking with plasma fatty acids measured in the third trimester and their association with Fetal Alcohol Spectrum Disorders (FASD). MethodsIn the parent study, moderate to heavy alcohol-using and low/unexposed comparison women were recruited during mid-pregnancy from two prenatal clinics in Ukraine. The participants’ live-born infants underwent physical and neurobehavioral exams prior to one-year of age. Infants were classified as having FASD if their mothers reported moderate to heavy alcohol consumption and the infant had at least one standardized score below 85 on the Bayley Scales of Infant Development II (BISD-II) with or without physical features of FASD. From the overall cohort, a subset of mother-child pairs was selected representing three groups of cases and controls: Alcohol-Exposed with FASD (n = 30), Alcohol-Exposed Normally Developing (n = 33), or low/unexposed Controls (n = 46). Third trimester maternal plasma samples were analyzed for fatty acids and levels were compared across groups. ResultsPlasma compositions of omega-6 fatty acids were altered in mothers with FASD infants compared to other groups. More specifically, the % of stearic acid (C18:0), arachidonic acid (AA, C20:4n6) and docosapentaenoic acid (DPAn6, C22:5n6) were significantly higher in mothers with FASD infants than low/unexposed controls or alcohol-exposed mothers with typically developing infants. Alcohol-exposed women who smoked had lower n3-docosapentaenoic acid (DPAn3, C22:5n3) and docosahexaenoic acid (DHA, C22:6n3) and higher DPAn6 than women consuming alcohol alone or abstainers. ConclusionsAlterations in fatty acid profiles were observed in moderate to heavy alcohol-consuming mothers with infants classified with FASD compared to alcohol-exposed typically developing infants or controls. These results support the idea that maternal fatty acid status can play a role in the etiology of FASD. Funding SourcesThis research was funded by support from NIH Research Grant and conducted in conjunction with the Collaborative Initiative on Fetal Alcohol Spectrum Disorders(CIFASD).