At the time that the U.K. and European Union reference intakes of folate shown in Table 10.3 were being discussed, the results of intervention trials for the prevention of neural tube defects (Section 10.9.4) were only just becoming available. At that time, there was no information concerning the effects of folate status onhyperhomocysteinemia (Section 10.3.4.2). The U.S./Canadian report (Institute of Medicine, 1998) notes specifically that protective effects with respect to neural tube defects were not considered relevant to the determination of the Dietary Reference Intake of folate, and there was insufficient evidence to associate higher intakes of folate (and lower plasma concentrations of homocysteine) with reduced risk of cardiovascular disease.
The total body pool of folate in adults is 17 f mol (7.5 mg), with a biological half-life of 101 days. This suggests a minimum requirement for replacement of 85 nmol (37 fig) per day (Herbert, 1987a). Studies of the urinary excretion of acetamido-p-aminobenzoyl glutamate in subjects maintained on folate-free diets suggest that there is catabolism of 170 nmol (80 f g) of folate per day.
Depletion/repletion studies to determine folate requirements using methyl-tetrahydrofolate suggest a requirement of the order of 170 to 220 nmol (80 to 100 f g) per day. However, because of the problems of determining the biological availability of the various folates found in foods (Section 10.2.1), reference intakes allow a wide margin of safety and are generally based on an allowance of 3 to 6 fg (7 to 14 nmol) per kg of body weight (200 to 400 f g per day for adults). In pregnancy and lactation, an additional 200 f g per day is generally recommended; this is probably more than can be obtained from foods, and therefore may require supplementation. As discussed in Section 10.9.4, supplements of400 f g of folic acid per day in addition to normal intake are recommended for reduction of the risk of neural tube defects.
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