Folate, a water-soluble B-type vitamin which is synthesized as folic acid, helps in the maintenance of new cells. As such, the name, which is derived from a Latin word meaning “leaf” is a common sight in general health and medical literature concerning infancy and pregnancy, where the division and growth of cells is of crucial import. (Herbert, 1999)
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Unsurprisingly, folate’s importance to cell division and growth is derived from its necessity to the production of DNA and RNA which are the core component of cells. Additionally, folate plays a role in regulation of cancer-inducing changes in DNA. (Fenech, et. al., 1998) Folate also plays a role in the metabolization of the amino acid known as homocysteine. (Kamen, 1997) Without folate, unchecked levels of homocysteine can lead to bone weakness and poses some cardiovascular risk. (Sato, et al; 2005) Still, this should not be misunderstood. Kaare Harald Bønaa, co-author of a report from the European Society of Cardiology, notes that based on results from the Norwegian Vitamin Trial, while folate does help lower the levels of homocysteine, it does not necessarily reduce the risk of heart failure. As such, high dose prescriptions of B-vitamins such as folate, do not prevent heart diseases and strokes, and are advisable only for patients suffering from B-vitamin deficiencies. (Bønaa, 2005)
The recommended dietary intake for folate is set by the Institute of Medicine of the National Academy of Sciences (1998) at 400 micrograms per day for adults of both genders. For pregnant or lactating women, the recommended dietary intake for folate is 500 micrograms daily for those in the age range of 14-18, and 600 micrograms daily for those aged 19 and above. No recommended dietary intake has been sufficiently established for infants by the Institute of Medicine. However, they have approximated an ‘adequate intake’ measure based on the amounts of folate consumed by healthy breast-fed infants. As such, the Institute of Medicine opines that 65 micrograms of folate is adequate for children up to 6 years old and 80 micrograms for children up to 12 years old. Incidentally, the Dietary Folate Equivalent of naturally occurring folate to synthetic folic acid derived from vitamin supplements and fortified foods. Effectively speaking, for every microgram of folate expressed in the recommended dietary intake, individuals may take 0.6 micrograms of folic acid from supplements and fortified foods instead.
Leafy vegetables such as lettuces, spinach and turnip greens are among the richest sources of folate, making it aptly the “leaf” vitamin. Other rich sources of folate include dried beans and peas and sunflower seeds. Many cereal products such as ready to eat whole grain cereals and white rice are also rich in folate, primarily due to having been artificially fortified with a quarter to a hundred per cent of the recommended dietary allowance for folic acid. Certain fruits such as oranges, tomatos, cantaloupes, papayas and bananas are also identified as rich sources of folate. (USDA, 2005)
Much of the attention given to folate revolves around the link between folate deficiencies in pregnant women and neural tube defects in their children. As such, health watchdog groups and government health departments around the world have repeatedly recommended the use of supplements for the purposes of addressing these deficiencies. As implied above, this has led to many countries such as Indonesia, Mongolia and various Middle Eastern nations in addition to the United States introducing vitamin fortification of folate into various food commodities such as flour and cereal. The European Union stands as a notable exception in that the Food Standards Agency of the United Kingdom only recommends folate-fortification, whilst the remainder of the EU has, at present, not made fortification mandatory. (Russell, 2006)
Gentili (2007) notes that the presence of folate is oft manifested in glutamate compounds which cannot be endogenously generated by the human physiognomy. The reason why folates manifest themselves in natural polyglutamate tissues is because it is a cell form that can sufficiently retain them. In terms of absorption and excretion, folates are metabolized into monoglutamates, which enable them to be transported across the human respiratory and excretory systems as plasma and urine. This metabolization occurs in the luman of the small intestine, where reside the enzymes that can convert the polyglutamate form of folates (i.e. food tissue) into the appropriate monoglutamate form. This monoglutamate form is then absorbed into the proximate area of the central small intestine or jejunum. Plasma-bound folate takes the form of 5-methyltetrahydrofolate or 5-methyl THFA, and is demethylated before it can be of any use to the human body in those enzymatic reactions which require folate.
Incidentally, this is why excess or toxic levels of folate intake have been associated with Vitamin B-12 deficiencies. For consumed folic acid and folate to be properly metabolized into an excretable form, cobalamin or B-12 is required. Without B-12, folate cannot be rendered into an excretable form and remains bound as 5-methyl THFA. As such, regardless of the side effects of the folate itself, excess folate intake can result in severe B-12 deficiency and as a result leads to difficulty in metabolizing other vitamins, as well as megaloblastic anemia may occur, as well as neurological and psychiatric abnormalities resulting from this deficiency (Scott, 1999)
As indicated above, many enzymatic reactions require folate acid, in its biologically active and metabolic form as THFA or demethyated tetrahyrofolic acid. This is because folate is necessary to the transfer of carbon units crucial to the synthesis of proteins and nucleic acids which form the base of DNA and RNA. (Fenech, et. al., 1998; Gentili, 2007) THFA also plays a necessary role in the synthesis of purine, thymidine and amino acid. From this, it is expected that folate deficiencies result in impairments in highly critical physiological functions: cell division, the impairment of methylatic reactions which regulate genetic expression. Hence, folate acid deficiency in pregnant women leads to severe developmental impairments in the prenatal infant.
Mulenga, et. al. (2006) also report that despite the critical importance of folate to prenatal growth of infants, the use of high dose folic acid supplements interfere with anti-malarial treatment, specifically, sulfacoxine-pyrimethamine. This is a controversial point to consider, as while 4 micrograms of folate per day is adequate to protect against neural tube and brain defects in the developing fetus, women in sub-Saharan Africa, where the study was conducted, often take up to 5 milligrams a day because that this is the dosage at which folate supplements are available. The study reported that while there was no difference in stillbirths, premature deliveries and neonatal deaths among the subjects, treatment failure was double among those women taking the folate supplements than those taking placebos or 0.4 mg of folate.
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