Folic acid, also known as pterylglutamic acid (PGA), is a vitamin in the group of vitamin B. Folic acid is converted to folate in the body. Unlike folate, folic acid itself is not found naturally in food, instead being consumed either through vitamin supplementation or by being added to foods such as flour, a process known as ‘fortification” of food. Folic acid is metabolised in the body to folate, also known as vitamin B9,1 vitamin Bc, or vitamin M.2 Folic acid is on the World Health Organisation’s list of essential medicines, which is a list of the most effective, and safe, medicines required to be in a well-functioning health system.
Folate deficiency is an example of a ‘micronutrient deficiency’3 alongside vitamin C deficiency (resulting in Scurvy) and vitamin D deficiency (resulting in Rickets) amongst many others. Consuming too little folate can lead to several conditions including anaemia, which often manifests by feeling tired and short of breath. There are several other causes of anaemia, which is covered extensively by Dr Etienne Ciantar in his article Anaemia in pregnancy. Insufficient folate consumption during pregnancy can result in even more serious and permanent health conditions in the unborn child. Specifically, folate deficiency during pregnancy can lead to neural tube defects (NTDs) such as anencephaly and spina bifida4. Anencephaly is when a part of the brain or skull is not formed during development of the unborn child, and most do not survive development to term to be born. Spina bifida is a birth defect where the neural tube fails to close in the first few weeks of development. Spina bifida results in the child’s spine and spinal cord not being fully developed and results in a number of health problems including bone defects, neurological disorders, bladder conditions (including recurrent infections) and poor educational attainment.
Neural tube defects such as those caused by folate deficiency are typically identified at the dating scan, usually done between 8 and 14 weeks into the pregnancy.
While the first suggestions that maternal intake of certain vitamins affected the risk of serious fetal malformations began in the 1960s, the first clinical trials identifying the role of folic acid in preventing NTDs were in 1991, where the authors found that if women took 4 mg of folic acid each day before and during the first trimester, this prevented approximately 80% of cases of NTDs.5 Current guidance is to take 4mg daily when trying to conceive and for the first 12 weeks of pregnancy, although some women will be advised to take a slightly larger dose of 5mg depending upon certain risk factors that their clinician will discuss with them. Despite this, a recent study looking at half a million women across England found that only 31% took folic acid supplements prior to pregnancy, 62% began taking folic acid once their pregnancy had been confirmed (albeit probably too late to prevent NTDs) and 8% didn’t take folic acid at any point during their pregnancy.6
As there is a significant portion of the population who do not take folic acid during the ‘at risk’ period, and given the serious nature of the potential effects upon the unborn child, many countries have taken steps to reduce this risk much further. Eighty-one countries across the world have now introduced fortification of flour with folic acid as a mandatory requirement. This step is not a replacement for folic acid supplementation but increases the baseline consumption of folate to reduce the risk across the population of folate deficiency in pregnancy. The countries that have embraced this have reported a subsequent reduction in the frequency of NTDs.7 Despite this, the UK and all countries across the European Union are yet to take this step due to concerns that some of the population may then be consuming too much folate. However, recent evidence suggests that an upper limit of folate consumption is ‘unnecessary’ and that no barriers now remain to implement the policy of folic acid fortification of flour to reduce the risk of two devastating conditions.8
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