Folate, absorption neural tube defect

Folic acid deficiency, unlike vitamin B12 deficiency, is often caused by inadequate dietary intake of folates. Alcoholics and patients with liver disease develop folic acid deficiency because of poor diet and diminished hepatic storage of folates. There is also evidence that alcohol and liver disease interfere with absorption and metabolism of folates. Pregnant women and patients with hemolytic anemia have increased folate requirements and may become folic acid-deficient, especially if their diets are marginal. Evidence implicates maternal folic acid deficiency in the occurrence of fetal neural tube defects, eg, spina bifida. (See Folic Acid Supplementation A Public Health Dilemma.) Patients with malabsorption syndromes also frequently develop folic acid deficiency. Folic acid deficiency is occasionally associated with cancer, leukemia, myeloproliferative disorders, certain chronic skin disorders, and other chronic debilitating diseases. Patients who require renal dialysis also develop folic acid deficiency, because folates are removed from the plasma each time the patient is dialyzed. 

Neuhouser, M.L. et al.. Absorption of dietary and supplemental folate in women with prior pregnancies with neural tube defects and controls, 7. Am. Coll. Nutr., 17, 625,1998. 

Folic acid deficiency caused by insufficient supply in the diet or by malfunction of absorptive processes is detected by a decrease in folic acid concentration in red blood cells and plasma, and by a change in blood cell patterns. There are clear indications that a congenital defect (neural tube defect) and a number of diseases are based on a deficiency of folate. 

There is some evidence that folate supplements in excess of 350 [ig/day may impair zinc absorption. In addition, there are two potential problems that have to be considered when advocating either widespread use of folate supplements or enrichment of foods with folate for protection against heart disease and neural tube defect ... 

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