Abstract
Since the early 1990s, maternal folic acid supplementation has been recommended prior to and during the first trimester of pregnancy, to reduce the risk of infant neural tube defects. In addition, many countries have also implemented the folic acid fortification of staple foods, in order to promote sufficient intakes amongst women of a childbearing age, based on concerns surrounding variable dietary and supplementation practices. As many women continue to take folic acid supplements beyond the recommended first trimester, there has been an overall increase in folate intakes, particularly in countries with mandatory fortification. This has raised questions on the consequences for the developing fetus, given that folic acid, a methyl donor, has the potential to epigenetically modify gene expression. In animal studies, folic acid has been shown to promote an allergic phenotype in the offspring, through changes in DNA methylation. Human population studies have also described associations between folate status in pregnancy and the risk of subsequent childhood allergic disease. In this review, we address the question of whether ongoing maternal folic acid supplementation after neural tube closure, could be contributing to the rise in early life allergic diseases.
Highlights
The dramatic increase in childhood allergic disease is a serious public health issue in high-income countries [1,2,3,4]
Folic acid acts as a methyl donor, with the capacity to alter the methylation of DNA
Folic acid has been found to modify gene expression, linked to the development of allergic disease in offspring. These actions of folic acid, coupled with results from several human population studies, provide some foundation to bring into question the role of folic acid exposure in late pregnancy in the development of allergic disease in children, after the critical period of time for protection against neural tube defects
Summary
The dramatic increase in childhood allergic disease is a serious public health issue in high-income countries [1,2,3,4]. Current evidence points to a multifactorial aetiology with a complex genetic predisposition, interacting with key environmental factors, including dietary changes. Both epidemiologic and mechanistic studies have linked specific and general consequences of recent dietary intake patterns, to biological effects in early life, including early immune dysregulation, an enhanced predisposition to inflammation, and inappropriate responses to normally harmless ubiquitous antigens, such as allergens, in very early life. The impact of diet is complex and is influenced through changing food sources and changes in specific nutrient intakes, with secondary immune and metabolic effects These nutritional factors (including folate) have the potential to induce persistent developmental changes in gene expression through epigenetic modifications, and thereby, alter developing immune pathways, organ systems, and subsequent disease predisposition [5,6,7]. One of the best described examples is the ability to modulate metabolic activity in response to the maternal nutrient
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