Thiamin deficiency on fetal brain development with and without prenatal alcohol exposure

Adequate thiamin levels are crucial for optimal health through maintenance of homeostasis and viability of metabolic enzymes, which require thiamine as a co-factor. Thiamin deficiency occurs during pregnancy when the dietary intake is inadequate or excessive alcohol is consumed. Thiamin deficiency leads to brain dysfunction because thiamin is involved in the synthesis of myelin and neurotransmitters (e.g., acetylcholine, [gamma]-aminobutyric acid, glutamate), and its deficiency increases oxidative stress by decreasing the production of reducing agents. Thiamin deficiency also leads to neural membrane dysfunction, because thiamin is a structural component of mitochondrial and synaptosomal membranes. Similarly, in-utero exposure to alcohol leads to fetal brain dysfunction, resulting in negative effects such as fetal alcohol spectrum disorder (FASD). Thiamin deficiency and prenatal exposure to alcohol could act synergistically to produce negative effects on fetal development; however, this area of research is currently under-studied. This minireview summarizes the evidence for the potential role of thiamin deficiency in fetal brain development, with or without prenatal exposure to alcohol. Such evidence may influence the development of new nutritional strategies for preventing or mitigating the symptoms of FASD. Key words: thiamin, brain, fetus, alcohol, fetal alcohol spectrum disorder. Des niveaux adequats de thiamine sont essentiels a une sante optimale en maintenant l'homeostasie et la viabilite des enzymes metaboliques qui utilisent la thiamine comme cofacteur. La deficience en thiamine durant la grossesse survient lorsque l'apport par la diete est insuffisant ou qu'une quantite excessive d'alcool est consommee. La deficience en thiamine mene a une dysfonction cerebrale a cause de son implication dans la synthese de la myeline et des neurotransmetteurs (p.ex. l'acetylcholine, l'acide 32 [gamma]-aminobutyrique, le glutamate) et elle accroit le stress oxydant en diminuant la production d'agents reducteurs. La deficience mene aussi au dysfonctionnement de la membrane neurale car la thiamine est une composante structurale des membranes mitochondriales et synaptiques. De la meme facon, l'exposition a l'alcool in utero provoque une dysfonction du cerveau foetal qui resulte en des effets indesirables tels les troubles du spectre de l'alcoolisation foetale (TSAF). Les consequences indesirables de la deficience en thiamine et de l'exposition prenatale a l'alcool pourraient resulter de leur action synergique sur le developpement foetal, mais ce domaine de recherche est sous-etudie. Cette synthese resume les preuves du role potentiel de la deficience en thiamine dans le developpement du cerveau foetal avec ou sans exposition prenatale a l'alcool. De telles preuves pourraient influencer le developpement de nouvelles strategies nutritionnelles pour prevenir ou attenuer les symptomes des TSAF. [Traduit par la Redaction] Mots-cles: thiamine, cerveau, foetus, alcool, troubles du spectre de l'alcoolisation foetale.
Introduction Maternal abuse of alcohol and its effect on the developing fetus has been widely studied for several decades. Prenatal alcohol consumption is associated with fetal alcohol spectrum disorder (FASD), [...]