Maternal
folate status is involved in the pathogenesis of neural tube defects (NTDs),
and although the exact mechanism is not clear, a nutritional or genetic defect
in homocysteine metabolism via methionine synthase appears likely. Women who
previously had infants with NTDs were found to have had higher plasma
homo-cysteine levels than women who had normal offspring.
Higher homocysteine levels can be indicative of the presence of a metabolic defect
that increases risk of NTDs or other congenital defects. The rapidly dividing
cells of the neural tube can be particularly sensitive to folate because of its
importance to methyl group metabolism in nucleic acid and amino acid biosynthesis.
Certainly,
the scientific evidence that folic acid taken around the time of conception
prevents many NTDs has been very strong. In Canada starting in January 1998,
flour and pasta were fortified with folic acid to help prevent NTDs, and
results have been very encouraging. In Europe, recommendations to increase
folic acid through voluntary supplementation did not reduce the incidence of
NTDs; however, food fortification had not been implemented.
Interestingly
enough, however, when physicians took an active role in promoting folic acid
supplementation, folic acid intake increased. Women who received folic acid counselling,
a 30-day supply of folic acid tablets, and a reminder telephone call increased
their folic acid intake by 68%, compared with 20% of controls who received only
a pamphlet on folic acid.
Periconceptional
use of folic acid has been shown to reduce the incidence of non-NTD birth
defects, such as cleft palates, upper limb reduction deficits, and
genitourinary defects. Others have also observed a link between folic acid and
congenital heart defects, urinary tract anomalies, orofacial clefts, limb
defects, and pyloric stenosis.
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