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Folate is a naturally occurring essential vitamin (vitamin B9) found in fruit, green leafy vegetables, grains and legumes.1 It is important in DNA and RNA synthesis and acts as an enzyme cofactor in the assembly of nucleic acids and amnio acids.1 Folic acid refers to a synthetic form, which is converted to folate following its consumption.1
Sufficient folate levels can only be achieved from satisfactory dietary intake or supplementation. Folate deficiency can be associated with other vitamin and mineral deficiencies. Certain public health systems (including the UK) have fortified certain foods (eg, breads, cereals) with folic acid. The aim is to reduce the risks of folate deficiency in pregnancy,2 as pregnancy is often unplanned and adherence to national folic acid supplementation guidelines is typically low. Pregnancy increases folate requirements, due to increased metabolic demands and fetal growth. Folate deficiency in pregnancy can result in anaemia in the mother, placental health issues, increased risk of early fetal loss, premature birth, fetal growth restriction and pre-eclampsia.3
Folate deficiency in pregnant mothers also significantly increases the risk of neural tube defects, other major congenital malformations and neurodevelopmental disorders including autism spectrum disorder.4 Putative mechanisms involve interference with DNA and RNA synthesis and biochemical pathway alterations, resulting in excess toxic metabolites.
The WHO recommends daily supplementation with 0.4 mg of folic acid to women in the general population who are planning a pregnancy or who are already pregnant to minimise the risks of malformations.5 A meta-analysis, which included one randomised controlled trial and three cohort studies, concluded that supplementation with lower doses of folic acid reduces the risk of neural tube defect by 62% in the general population.6 Based on the results of three randomised controlled trials, the same authors reported that supplementation with higher doses …
Footnotes
Twitter @MOP_Kinney
Contributors MOK and ND wrote sections of the original manuscript. All authors were involved in editing the original submission and the revised submission.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests MOK has received salary support from UCB to allow a period of elective work and speaker fees from Eisai and Angelini Pharma. JJC has received grants to undertake research and honoraria for giving lectures from UCB-Pharma, Sanofi-Synthelabo, GlaxoSmithKline, Janssen-Cilag, Pfizer and Eisai. ND has served on advisory boards and has received consultancy fees from UNEEG medical, Arvelle Therapeutics, Eisai, Sanofi and UCB Pharma.
Provenance and peer review Commissioned. Externally peer reviewed by Tony Marson, Liverpool, UK, and Angela O’Neal, Boston, USA.
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