Component
Genomic DNA methylation
DNA cytosine methylation; retain cell and assay scope.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Seven weeks at 115 micrograms DFE/day produced a nonsignificant tendency toward increased DNA methyl acceptance (P=0.08).
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Young MTHFR 677CC/TT women; controlled folate feeding.
- limitations
- Assay-specific trend, not demonstrated global hypomethylation.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Homo sapiens
- plain_language
- This result suggested but did not establish a methylation decrease.
- primary_references
- [shelnutt-2004] Methylenetetrahydrofolate reductase 677C-->T polymorphism affects DNA methylation in response to controlled folate intake in young women (2004). https://pubmed.ncbi.nlm.nih.gov/15350988/ DOI: 10.1016/j.jnutbio.2004.04.003
- tissue_or_cell_type
- Blood-derived genomic DNA
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 789–798
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Young MTHFR 677CC/TT women; controlled folate feeding. · source_derived_draft · unverified_draft
### folate-methyl-young-dna-trend Seven weeks at 115 micrograms DFE/day produced a nonsignificant tendency toward increased DNA methyl acceptance (P=0.08). Condition category: nutrient_deficiency nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: This result suggested but did not establish a methylation decrease. organism: Homo sapiens tissue_or_cell_type: Blood-derived genomic DNA experimental_model: Young MTHFR 677CC/TT women; controlled folate feeding. limitations: Assay-specific trend, not demonstrated global hypomethylation. [shelnutt-2004] Methylenetetrahydrofolate reductase 677C-->T polymorphism affects DNA methylation in response to controlled folate intake in young women (2004). https://pubmed.ncbi.nlm.nih.gov/15350988/ DOI: 10.1016/j.jnutbio.2004.04.003
Complete structured claim and evidenceDuring 400 micrograms DFE/day repletion, DNA methylcytosine:total-cytosine increased significantly only in MTHFR 677TT women.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Young MTHFR 677CC/TT women; controlled folate feeding.
- exposure
- Seven weeks after depletion
- limitations
- Within-group significance alone does not establish a genotype interaction.
- nutrient_topic
- Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. · Folate (vitamin B9)
- organism
- Homo sapiens
- plain_language
- The directly measured DNA-base response differed across genotype groups.
- primary_references
- [shelnutt-2004] Methylenetetrahydrofolate reductase 677C-->T polymorphism affects DNA methylation in response to controlled folate intake in young women (2004). https://pubmed.ncbi.nlm.nih.gov/15350988/ DOI: 10.1016/j.jnutbio.2004.04.003
- tissue_or_cell_type
- Blood-derived genomic DNA
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Folate and folic acid: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 800–810
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Young MTHFR 677CC/TT women; controlled folate feeding. · source_derived_draft · unverified_draft
### folate-methyl-young-tt-repletion During 400 micrograms DFE/day repletion, DNA methylcytosine:total-cytosine increased significantly only in MTHFR 677TT women. Condition category: nutrient_deficiency nutrient_topic: Folate and folic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The directly measured DNA-base response differed across genotype groups. organism: Homo sapiens tissue_or_cell_type: Blood-derived genomic DNA experimental_model: Young MTHFR 677CC/TT women; controlled folate feeding. limitations: Within-group significance alone does not establish a genotype interaction. exposure: Seven weeks after depletion [shelnutt-2004] Methylenetetrahydrofolate reductase 677C-->T polymorphism affects DNA methylation in response to controlled folate intake in young women (2004). https://pubmed.ncbi.nlm.nih.gov/15350988/ DOI: 10.1016/j.jnutbio.2004.04.003
Complete structured claim and evidence
Where it participates (unsigned role)
After vitamin C derivative treatment, numerous mouse ESC promoters lost methylcytosine; imprinted regions and IAP retroelements were relatively resistant, so the effect was not indiscriminate erasure of genomic methylation.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Figure 2; resistant-region analysis
- experimental_model
- Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation
- exposure
- 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling.
- limitations
- Locus-selective cell-culture result; promoter demethylation did not automatically activate every affected gene.
- nutrient_topic
- Vitamin C research collection; topical membership is not evidence of a direct dietary effect. · Vitamin C
- organism
- Mus musculus
- plain_language
- Vitamin C changed selected DNA methylation patterns in these cells; protected regions retained their marks.
- primary_references
- [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
- tissue_or_cell_type
- Embryonic stem cells
Vitamin C: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 991–1003
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation · source_derived_draft · unverified_draft
### c-reg-esc-promoter-demethylation After vitamin C derivative treatment, numerous mouse ESC promoters lost methylcytosine; imprinted regions and IAP retroelements were relatively resistant, so the effect was not indiscriminate erasure of genomic methylation. Condition category: normal nutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin C changed selected DNA methylation patterns in these cells; protected regions retained their marks. organism: Mus musculus tissue_or_cell_type: Embryonic stem cells experimental_model: Mouse Oct4-GiP ESCs in feeder-free 2i/LIF medium; DNA dot blot and hydroxymethyl-DNA immunoprecipitation; mC-DIP sequencing/qPCR and bisulfite validation limitations: Locus-selective cell-culture result; promoter demethylation did not automatically activate every affected gene. exposure: 100 µg/mL L-ascorbic acid 2-phosphate (A8960), medium replaced daily; 12-h and 72-h sampling. cross_nutrient: false evidence_location: Figure 2; resistant-region analysis [c-reg-blaschke] Vitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23812591/ DOI: 10.1038/nature12362
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.