Prenatal Alcohol Exposure and Congenital Heart Defects: Retinoic Acid Deficiency as a Potential Mechanism in Dextro-Type Transposition of the Great Arteries

TL;DR

This paper explores how alcohol exposure during pregnancy may cause heart defects in babies by reducing a key chemical called retinoic acid.

Contribution

The paper proposes a new mechanism linking alcohol exposure to d-TGA through retinoic acid deficiency.

Findings

Prenatal alcohol exposure is associated with dextro-type transposition of the great arteries.

Ethanol may interfere with retinoic acid biosynthesis, leading to developmental heart defects.

Abstract

Fetal alcohol spectrum disorder (FASD) is a preventable cause of developmental disabilities linked to prenatal alcohol exposure (PAE). Congenital heart defects (CHDs) are frequently observed in FASD, with a notable association between PAE and dextro-type transposition of the great arteries (d-TGA). A potential pathogenetic mechanism of d-TGA in FASD, involving retinoic acid (RA) deficiency due to the interference of ethanol with RA biosynthesis, is proposed. Further investigation is required to understand the timing and impact of alcohol exposure on congenital anomalies, particularly in the context of CHDs.

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