Preconception paternal ethanol exposures induce alcohol-related craniofacial growth deficiencies in fetal offspring

Abstract:

Fetal Alcohol Syndrome (FAS) is characterized by a range of structural birth defects, including facial dysmorphia, central nervous system growth deficits (microcephaly), and prenatal/postnatal growth restriction, which correlate with the magnitude of prenatal alcohol exposure (1, 2).

Although exclusively attributed to the maternal consumption of alcohol during pregnancy, multiple clinical studies and case reports have emerged describing instances where infants presenting with alcohol-related birth defects were born to mothers who denied consuming alcohol during pregnancy (2, 3). For example, the Collaboration on FASD Prevalence (CoFASP) research consortium recently conferred a diagnosis of FAS to a cohort of 41 children whose mothers refused to endorse alcohol use during pregnancy (3).

The prevailing rationalization for these reported inconsistencies is that the mothers did not faithfully report their prenatal alcohol use (4). However, the recent identification of epigenetic mechanisms of paternal inheritance presents an alternative explanation; that the drinking habits of the birth father may contribute to the emergence of alcohol-related phenotypes in their offspring.

However, due to the misconception that sperm do not transmit information beyond the genetic code, the influence of paternal drinking on the development of alcohol-related birth defects has not been rigorously examined.

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In 1981, the U.S. Surgeon General issued a public health advisory warning that alcohol use by women during pregnancy could cause birth defects.

Since this time, maternal alcohol use during pregnancy has remained the sole explanation for alcohol-related birth defects. In contrast, paternal drinking and lifestyle choices remain unexamined.

Using a physiologically relevant mouse model, our studies are the first to demonstrate that male drinking is a plausible yet completely unexamined factor in the development of alcohol related craniofacial abnormalities and growth deficiencies.

Our study demonstrates the critical need to target both parents in pre-pregnancy alcohol messaging and to expand epidemiological studies to measure the contributions of paternal alcohol use on children's health.