To explore the mechanisms of paternal contributions to fetal alcohol spectrum disorders
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abstract
Clinical studies report that 75% of fetal alcohol spectrum disorder (FASD) children have biological fathers who were either heavy drinkers or chronic alcoholics. However, the role of male alcohol use in the development of fetal alcohol syndrome birth defects remains unexplored. This is largely due to the misconception that sperm do not transmit heritable information beyond the genetic code. Using a mouse model, investigators at Texas A&M University have linked preconception male alcohol use to fetal growth restriction, placental dysfunction, and long-term deficits in the metabolic health of the adult offspring. These phenotypes are similar to those reported in children with FASD and reveal male alcohol use to be an unrecognized contributing factor in the development of alcohol-induced growth defects. Using state-of-the-art sequencing technologies, this project aims to define the epigenetic mechanisms by which alcohol-induced errors in developmental programming transmit to the offspring and determine how long these environmentally induced effects persist after the males stop drinking. Subsequently, the investigators will examine why the offspring of alcohol-exposed males become growth restricted. This proposal challenges the prevailing paradigm, which exclusively focuses on maternal alcohol exposures and examines a novel hypothesis that considers paternal contributions to FASD birth defects. This study will be among the first to explore the role of sperm-inherited alterations in epigenetic programming in the development of a pediatric disorder and will develop biomarkers of exposure that will offer the opportunity to significantly enhance the health of future pregnancies.
