Altered Developmental Programming in a Dual Model of Maternal and Paternal Alcohol Consumption

Abstract

According to the CDC, Fetal Alcohol Spectrum Disorders (FASDs) are a group of conditions that can occur in a person whose mother drank alcohol during pregnancy. This definition places the fault for FASD‐associated mental and physical defects exclusively on the mother. However, emerging research can now link preconception paternal environmental exposures and lifestyle choices with several disease states within the offspring. Despite the efforts to recognize paternal epigenetic contributions, research examining congenital disabilities is limited and remains exclusively focused on maternal exposures. We hypothesized that FASD‐associated developmental defects would become exacerbated in a dual parental model of alcohol consumption. To investigate the contributions of dual parental ethanol (EtOH) exposure on offspring development, we exposed C57BL/6J adult [postnatal day (PND) 90] males and females to either control or alcohol (10% EtOH) treatments using the Drinking in the Dark (DID) method. After a preconception treatment period of 6 weeks for males and ten days for females, we mated exposed mice. Pregnancies were confirmed by weight gain at gestational day (GD) 10. Pregnant females ceased alcohol treatments at gestational day ten, and we terminated pregnancies at either GD 16.5 or 18.5. We examined morphometric measures of fetal development and 2D images of the placenta and craniofacial features. From these studies, we find that each exposure source (maternal, paternal, or dual parental) exhibits its unique growth and craniofacial phenotype. This finding draws attention to the need for a thorough investigation of both parents' exposure history when determining the child's overall health status. It also emphasizes that the presence of a defect does not mean that the blame lies solely with the mother. Instead, it might be the combinatorial effect of both parents' life exposures before conception.