Neural tube defects, vitamins and homocysteine

Eur J Pediatr. 1998 Apr:157 Suppl 2:S139-41. doi: 10.1007/pl00014299.

Abstract

Folic acid (multivitamins) reduce the recurrence and occurrence of neural tube defects (NTDs). Vitamin profiles seem not suitable to identify women at risk for NTDs. A subset of these women have hyperhomocysteinaemia and a mutation of the gene for thermolabile methylenetetrahydrofolate reductase (MTHFR). From studies with the rat embryo in vitro, it can be concluded that the de- and remethylation cycle of methionine, being folate and vitamin B12 dependent, is crucial for embryonic and fetal growth probably via generation of DNA, proteins and polyamines. Nutrition for the embryo is also supplied by the follicular fluid, the yolk sac, the extraembryonic coelomic cavity and the amniotic fluid.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Female
  • Folic Acid / blood
  • Folic Acid / metabolism
  • Homocysteine / blood
  • Homocysteine / metabolism*
  • Humans
  • Methionine / metabolism
  • Methylation
  • Methylenetetrahydrofolate Reductase (NADPH2)
  • Mutation
  • Neural Tube Defects / metabolism
  • Neural Tube Defects / physiopathology*
  • Neural Tube Defects / prevention & control
  • Oxidoreductases Acting on CH-NH Group Donors / genetics
  • Oxidoreductases Acting on CH-NH Group Donors / metabolism
  • Rats
  • Spinal Dysraphism / metabolism

Substances

  • Homocysteine
  • Folic Acid
  • Methionine
  • Oxidoreductases Acting on CH-NH Group Donors
  • Methylenetetrahydrofolate Reductase (NADPH2)