Fetal Alcohol Syndrome (FAS) is, sadly, a common finding worldwide.
Development of the face and brain are intimately interrelated, as the brain provides structural, cellular, and molecular input that guides the development of the face. The alcohol-exposed neonate presents with several structural birth defects including facial dysmorphia, central nervous system growth deficits (microcephaly), and prenatal/postnatal growth restriction. When seen, the mother is assumed to have consumed alcohol throughout her pregnancy. In fact, it is written into the CDC diagnostic criteria.
The pattern in FAS includes growth deficits (height and/or weight ≤10%), microcephaly (head (occipito-frontal) circumference ≤10%), and at least 2 of 3 facial features (short palpebral fissures below the 10th centile a smooth philtrum, and a narrow and poorly shaped vermillion border of the upper lip). In addition, other dysmorphic features known to occur more frequently in patients with PAE include ptosis of the eyelids, epicanthal folds, midface hypoplasia, a short anteverted nose, a long philtrum, abnormally shaped “railroad track” ears, abnormal hand creases, particularly the hockey stick crease, limited finger extension (camptodactilies), incomplete pronosupination of the elbows, and contractures in other joints. - Teratology Primer
However, we now have multiple studies and case reports where infants manifesting parental alcohol-related birth defects were born to mothers who emphaticly denied consuming alcohol during pregnancy. If so, then the paternal contribution must be examined.
The defects in the mouse are similar to those seen in humans. A recent study utilized a multiplex mouse model to test the hypothesis that: 1. preconception male alcohol exposures induce alcohol-related craniofacial defects and, 2. determine if paternal alcohol use can increase the penetrance and severity of alcohol-related phenotypes induced by maternal drinking.
Across a 2x2 factorial design, they measured alcohol-induced developmental defects in offspring generated with maternal (MatExp), paternal (PatExp), and dual parental (DualExp) models of alcohol exposure, using established scales for alcohol-induced craniofacial defects.
Paternal and dual-parental alcohol exposures induced significant reductions in offspring head size, ocular size, midfacial depth, and snout-occipital distance. Reductions in ocular size localized predominately to the right side.
A dose-response analysis, correlated the offspring snout-occipital distance and bodyweight-normalized brain weights, with the parental average daily ethanol dose (g/kg). Significant correlation was found between both measures and parental alcohol dose for male offspring across the PatExp and DuelExp treatments. In contrast, for the female offspring, a significant interaction was with the MatExp and DualExp treatments.
The inflection point past which paternal alcohol exposures induce significant craniofacial and central nervous system growth deficiencies, was at 2.9 g/kg, similar to that determined for maternal exposures.
Thus, the conclusion is quite sobering; both parents must abstain from excessive alcohol consumption when conceiving a child. And the mother must continue to abstain while gestating the fetus.
For the sake of the child, please all strive.
REFERENCES
KN Thomas et al. Preconception paternal ethanol exposures induce alcohol-related craniofacial growth deficiencies in fetal offspring, Journal of Clinical Investigation (2023). DOI: 10.1172/JCI167624
Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis https://bpb-ca-c1.wpmucdn.com/sites.uoguelph.ca/dist/f/94/files/2019/12/FAS_guidelines_accessible-P-1.pdf
M del Campo, KL Jones. Teratology Primer, 3rd Edition www.teratology.org/primer
What Are the Effects of Alcohol Use During Pregnancy? https://birthdefectsresearch.org/primer/fas.asp
An amazing long-known, little mentioned too common, condition. Booze. I'm so thankful it never much appealed to me.