Neural Tube Defects, Folic Acid and Methylation

Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid. To...

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Bibliographic Details
Published inInternational journal of environmental research and public health Vol. 10; no. 9; pp. 4352 - 4389
Main Authors Imbard, Apolline, Benoist, Jean-François, Blom, Henk
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 17.09.2013
MDPI
Subjects
Animals
Birth defects
Choline - metabolism
DNA methylation
Folic Acid - metabolism
Folic Acid - therapeutic use
Homocysteine - metabolism
Humans
Methylation
Neural Tube Defects - genetics
Neural Tube Defects - metabolism
Neural Tube Defects - prevention & control
Neurulation
Review
Vitamin B
Vitamin B 12 - metabolism
Vitamin B Complex - metabolism
Vitamin B Complex - therapeutic use
Vitamin deficiency
Online AccessGet full text
ISSN1660-4601
1661-7827
1660-4601
DOI10.3390/ijerph10094352

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Abstract Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid. To date, animal studies have not provided sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs. However, several lines of evidence suggest that not only folates but also choline, B12 and methylation metabolisms are involved in NTDs. Decreased B12 vitamin and increased total choline or homocysteine in maternal blood have been shown to be associated with increased NTDs risk. Several polymorphisms of genes involved in these pathways have also been implicated in risk of development of NTDs. This raises the question whether supplementation with B12 vitamin, betaine or other methylation donors in addition to folic acid periconceptional supplementation will further reduce NTD risk. The objective of this article is to review the role of methylation metabolism in the onset of neural tube defects.
AbstractList Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid. To date, animal studies have not provided sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs. However, several lines of evidence suggest that not only folates but also choline, B12 and methylation metabolisms are involved in NTDs. Decreased B12 vitamin and increased total choline or homocysteine in maternal blood have been shown to be associated with increased NTDs risk. Several polymorphisms of genes involved in these pathways have also been implicated in risk of development of NTDs. This raises the question whether supplementation with B12 vitamin, betaine or other methylation donors in addition to folic acid periconceptional supplementation will further reduce NTD risk. The objective of this article is to review the role of methylation metabolism in the onset of neural tube defects. [PUBLICATION ABSTRACT]
Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid. To date, animal studies have not provided sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs. However, several lines of evidence suggest that not only folates but also choline, B12 and methylation metabolisms are involved in NTDs. Decreased B12 vitamin and increased total choline or homocysteine in maternal blood have been shown to be associated with increased NTDs risk. Several polymorphisms of genes involved in these pathways have also been implicated in risk of development of NTDs. This raises the question whether supplementation with B12 vitamin, betaine or other methylation donors in addition to folic acid periconceptional supplementation will further reduce NTD risk. The objective of this article is to review the role of methylation metabolism in the onset of neural tube defects.
Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid. To date, animal studies have not provided sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs. However, several lines of evidence suggest that not only folates but also choline, B12 and methylation metabolisms are involved in NTDs. Decreased B12 vitamin and increased total choline or homocysteine in maternal blood have been shown to be associated with increased NTDs risk. Several polymorphisms of genes involved in these pathways have also been implicated in risk of development of NTDs. This raises the question whether supplementation with B12 vitamin, betaine or other methylation donors in addition to folic acid periconceptional supplementation will further reduce NTD risk. The objective of this article is to review the role of methylation metabolism in the onset of neural tube defects.Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid. To date, animal studies have not provided sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs. However, several lines of evidence suggest that not only folates but also choline, B12 and methylation metabolisms are involved in NTDs. Decreased B12 vitamin and increased total choline or homocysteine in maternal blood have been shown to be associated with increased NTDs risk. Several polymorphisms of genes involved in these pathways have also been implicated in risk of development of NTDs. This raises the question whether supplementation with B12 vitamin, betaine or other methylation donors in addition to folic acid periconceptional supplementation will further reduce NTD risk. The objective of this article is to review the role of methylation metabolism in the onset of neural tube defects.
Author Blom, Henk
Imbard, Apolline
Benoist, Jean-François
AuthorAffiliation 2 Metabolic Unit, Department of Clinical Chemistry, VU Free University Medical Center, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands; E-Mail: h.blom@vumc.nl
1 Biochemistry-Hormonology Laboratory, Robert Debré Hospital, APHP, 48 bd Serrurier, Paris 75019, France; E-Mail: jean-francois.benoist@rdb.aphp.fr
AuthorAffiliation_xml – name: 1 Biochemistry-Hormonology Laboratory, Robert Debré Hospital, APHP, 48 bd Serrurier, Paris 75019, France; E-Mail: jean-francois.benoist@rdb.aphp.fr
– name: 2 Metabolic Unit, Department of Clinical Chemistry, VU Free University Medical Center, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands; E-Mail: h.blom@vumc.nl
Author_xml – sequence: 1
  givenname: Apolline
  surname: Imbard
  fullname: Imbard, Apolline
– sequence: 2
  givenname: Jean-François
  surname: Benoist
  fullname: Benoist, Jean-François
– sequence: 3
  givenname: Henk
  surname: Blom
  fullname: Blom, Henk
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24048206$$D View this record in MEDLINE/PubMed
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Snippet Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is...
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proquest
pubmed
crossref
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Enrichment Source
StartPage 4352
SubjectTerms Animals
Birth defects
Choline - metabolism
DNA methylation
Folic Acid - metabolism
Folic Acid - therapeutic use
Homocysteine - metabolism
Humans
Methylation
Neural Tube Defects - genetics
Neural Tube Defects - metabolism
Neural Tube Defects - prevention & control
Neurulation
Review
Vitamin B
Vitamin B 12 - metabolism
Vitamin B Complex - metabolism
Vitamin B Complex - therapeutic use
Vitamin deficiency
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Title Neural Tube Defects, Folic Acid and Methylation
URI https://www.ncbi.nlm.nih.gov/pubmed/24048206
https://www.proquest.com/docview/1467988403
https://www.proquest.com/docview/1434743702
https://www.proquest.com/docview/1500779833
https://pubmed.ncbi.nlm.nih.gov/PMC3799525
Volume 10
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