Vitamins >> Vitamin B9 (Folic acid) Deficiency

Causes

Folate deficiency occurs in a number of situations. For example, low dietary intake and diminished absorption, as in alcoholism, can result in a decreased supply of folate. Certain conditions like pregnancy or cancer result in increased rates of cell division and metabolism, leading to an increase in the body's demand for folate.  Several medications may also contribute to deficiency.

Symptoms

Individuals in the early stages of folate deficiency may not show obvious symptoms, but blood levels of homocysteine may increase.  Rapidly dividing cells are most vulnerable to the effects of folate deficiency.  When the folate supply to the rapidly dividing cells of the bone marrow is inadequate, blood cell division becomes abnormal resulting in fewer but larger red blood cells.  This type of anemia is called megaloblastic or macrocytic anemia, referring to the large immature red blood cells. Neutrophils, a type of white blood cell, become hypersegmented, a change which can be found by examining a blood sample microscopically. Because normal red blood cells have a lifetime in the circulation of approximately four months, it can take months for folate deficient individuals to develop the characteristic megaloblastic anemia.  Progression of such an anemia leads to a decreased oxygen carrying capacity of the blood and may ultimately result in symptoms of fatigue, weakness, and shortness of breath.  It is important to point out that megaloblastic anemia resulting from folate deficiency is identical to the megaloblastic anemia resulting from vitamin B₁₂ deficiency, and further clinical testing is required to diagnose the true cause of megaloblastic anemia.

The Recommended Dietary  Allowance (RDA)

Determination of the RDA: Traditionally, the dietary folate requirement was defined as the amount needed to prevent a deficiency, severe enough to cause symptoms like anemia. The most recent RDA (1998) was based primarily on the adequacy of red blood cell folate concentrations at different levels of folate intake, which have been shown to correlate with liver folate stores.  Maintenance of normal blood homocysteine levels, an indicator of one-carbon metabolism, was considered only as an ancillary indicator of adequate folate intake.  Because pregnancy is associated with a significant increase in cell division and other metabolic processes requiring folate coenzymes, the RDA for pregnant women is considerably higher than for women who are not pregnant.  However, the prevention of neural tube defects (NTD) was not taken into consideration in setting the RDA for pregnant women. Rather, reducing the risk of NTD was considered in separate recommendation for women capable of becoming pregnant, because the crucial events in the development of the neural tube occur before many women are aware that they are pregnant.

Dietary Folate Equivalents (DFE): When the Food and Nutrition Board of the Institute of Medicine set the new dietary recommendation for folate, they introduced a new unit, the Dietary Folate Equivalent (DFE).  Use of the DFE reflects the higher bioavailability of synthetic folic acid found in supplements and fortified foods compared to that of naturally occurring food folates.

For example, a serving of food containing 60 mcg of folate would provide 60 mcg of DFE, while a serving of pasta fortified with 60 mcg of folic acid would provide 1.7 x 60 = 102 mcg DFE due to the higher bioavailability of folic acid.  A folic acid supplement of 400 mcg taken on an empty stomach would provide 800 mcg of DFE.

Genetic variation in folate requirements

A common polymorphism or variation in the gene for the enzyme methylene tetrahydrofolate reductase (MTHFR), known as the C677T MTHFR polymorphism, results in a less stable enzyme.  Depending on the population, 50% may have inherited one copy (C/T) and 5 to 25 % may have inherited two copies (T/T) of the abnormal MTHFR gene. MTHFR plays an important role in maintaining the specific folate coenzyme required to form methionine from homocysteine. When folate intake is low, individuals who are homozygous (T/T) for the abnormal gene have lower levels of the MTHFR enzyme and higher levels of homocysteine in their blood .  Improved folate nutritional status appears to stabilize the MTHFR enzyme, resulting in improved enzyme levels and lower homocysteine levels. An important unanswered question about folate is whether the present RDA is enough to normalize MTHFR enzyme levels in individuals who are homozygous for the C677T polymorphism, or whether those individuals have a higher folate requirement than the RDA.

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