A meta-analysis of the MTHFR C677T polymorphism and schizophrenia risk

Lewis et al., 2005 | Am J Med Genet B Neuropsychiatr Genet | Meta Analysis

Citation

Lewis Sarah J, Zammit Stanley, ... Smith George Davey. A meta-analysis of the MTHFR C677T polymorphism and schizophrenia risk. Am J Med Genet B Neuropsychiatr Genet. 2005-May-05;135B(1):2-4

Abstract

Epigenetic mechanisms such as methylation of DNA, could lead to abnormal neurodevelopment and may be important in the etiology of schizophrenia. Maternal dietary folate intake may play a role in determining methylation levels. The MTHFR gene C677T polymorphism influences folate metabolism and intracellular availability of folate metabolites for methylation. We carried out a meta-analysis of MTHFR C677T genotype and schizophrenia risk, and found that TT homozygotes had a significantly increased risk, OR 1.48 (1.18-1.86). This supports the hypothesis that folate status is a determinant of schizophrenia risk. Larger studies of this issue are required, together with studies of maternal genotype which could identify whether maternal folate status during pregnancy is important.

Key Findings

Larger studies of this issue are required, together with studies of maternal genotype which could identify whether maternal folate status during pregnancy is important.

Outcomes Measured

  • Requires manual extraction

Population

Field Value
Population See abstract
Sample Size See abstract
Age Range See abstract
Condition See abstract

MeSH Terms

  • Alleles
  • Female
  • Gene Frequency
  • Genotype
  • Humans
  • Male
  • Methylenetetrahydrofolate Reductase (NADPH2)
  • Polymorphism, Genetic
  • Risk Factors
  • Schizophrenia

Evidence Classification

  • Level: Meta Analysis
  • Publication Types: Journal Article, Meta-Analysis
  • Vertical: folate

Provenance

  • PMID: 15729744
  • DOI: (not available)
  • PMCID: Not in PMC
  • Verified: 2026-04-09 via PubMed E-utilities API

Source extracted via PubMed E-utilities API on 2026-04-09