Evidence map›Paper›PMID 28598562›Full record

ReviewCongenital anomalies2017

Genetic polymorphisms and folate status.

Mami Hiraoka, Yasuo Kagawa

Open access · hybridAbstract readReview
In one paragraph

Review in Congenital anomalies, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 9 pooled it
11.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 9 syntheses or guidelines pooled it, 172 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Pooled it
  9. Pooled it
  10. Trial
  11. Artificial intelligence for personalized multiple micronutrient supplementation in maternal health.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Mami HiraokaCollege of Nursing and Nutrition, School of Nutrition, Shukutoku University, Chiba City, Chiba, Japan.ORCID http://orcid.org/0000-0002-7433-7613
Yasuo KagawaDepartment of Medical Chemistry, Kagawa Nutrition University, Sakado City, Saitama, Japan.
Kagawa Nutrition University · JPShukutoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Moderate hyperhomocysteinemia-induced low folate status is an independent risk factor for cardiovascular disease, dementia, and depression. Folate is an essential cofactor in the one-carbon metabolism pathway and is necessary in amino acid metabolism, purine and thymidylate synthesis, and DNA methylation. In the folate cycle and homocysteine metabolism, folate, vitamin B12, vitamin B6, and vitamin B2 are important cofactors. Many enzymes are involved in folate transport and uptake, the folate pathway, and homocysteine (Hcy) metabolism, and various polymorphisms have been documented in these enzymes. Serum folate and total Hcy (tHcy) levels are influenced by folate intake and genetic polymorphisms in 5,10-methylenetertahydrofolate reductase (MTHFR) such as C677T. The prevalence of the MTHFR 677TT genotype varies across ethnic groups and regions, with a frequency of approximately 15% in Japanese populations. Individuals with the TT genotype have significantly higher tHcy levels and lower folate levels in serum than those with the CT and TT genotypes. However, administration of folic acid has been shown to eliminate these differences. Moreover, data have suggested that interventions based on genotype may be effective for motivating individuals to change their lifestyle and improve their nutrition status. Accordingly, in this review, we discuss the effects of MTHFR C677T polymorphisms on serum tHcy and folate levels with folic acid intervention and evaluate approaches for overcoming folic acid deficiency and related symptoms.

Indexed as

Dietary SupplementsPolymorphism, GeneticFemaleFolic AcidFolic Acid DeficiencyGene ExpressionGenotypeHumansHyperhomocysteinemiaMaleMetabolic Networks and PathwaysMethylenetetrahydrofolate Reductase (NADPH2)Middle AgedVitamin B 12Folic AcidMethylenetetrahydrofolate Reductase (NADPH2)MTHFR protein, humanVitamin B 12folatemethylenetetrahydrofolate reductasepersonalized nutritionpolymorphism

Identifiers

PMID28598562
PMCPMC5601299
OpenAlexW2624567430

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.