Component

Phylloquinone

Vitamin K1; distinct from menaquinones and menadione. Phylloquinone / vitamin K1. Read linked claims for the population, experiment and limits.

10 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Dietary K1 restriction reduced prothrombin and osteocalcin gamma-carboxylation and lowered plasma K1 and urinary Gla excretion.

    Phylloquinone → Vitamin K-dependent protein gamma-carboxylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"}
    experimental_model
    Metabolic-unit dietary depletion/repletion
    exposure
    K1 restricted to 18 micrograms/day for 28 days, then stepped repletion
    limitations
    The measured endpoint is carboxylation, not an observed clinical clotting failure; restricted-K1 exposure does not define isolated K2 deficiency.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    21 women aged 60–80 years
    plain_language
    A shortfall can appear in protein-modification markers before it is described as a clinical syndrome.
    primary_references
    [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    tissue_or_cell_type
    Hepatic and extrahepatic protein markers
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 1007–1018

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolic-unit dietary depletion/repletion · source_derived_draft · unverified_draft

    ### k2-dietary-k-prothrombin Dietary K1 restriction reduced prothrombin and osteocalcin gamma-carboxylation and lowered plasma K1 and urinary Gla excretion. Condition category: nutrient_deficiency nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shortfall can appear in protein-modification markers before it is described as a clinical syndrome. organism: 21 women aged 60–80 years tissue_or_cell_type: Hepatic and extrahepatic protein markers experimental_model: Metabolic-unit dietary depletion/repletion limitations: The measured endpoint is carboxylation, not an observed clinical clotting failure; restricted-K1 exposure does not define isolated K2 deficiency. exposure: K1 restricted to 18 micrograms/day for 28 days, then stepped repletion evidence_span: {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"} [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    Complete structured claim and evidence

  2. Prothrombin carboxylation normalized at 200 micrograms/day, whereas other vitamin K markers had not all returned to baseline after short repletion up to 450 micrograms/day.

    Phylloquinone → Vitamin K-dependent protein gamma-carboxylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"}
    experimental_model
    Metabolic-unit dietary depletion/repletion
    exposure
    K1 restricted to 18 micrograms/day for 28 days, then stepped repletion
    limitations
    K1 restriction probes shared vitamin K status, not an isolated dietary K2 requirement. Biochemical undercarboxylation is not equivalent to clinical bleeding or fractures.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    21 women aged 60–80 years
    plain_language
    A liver-related marker can recover before an extrahepatic marker.
    primary_references
    [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    tissue_or_cell_type
    Hepatic and extrahepatic protein markers
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 1020–1031

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolic-unit dietary depletion/repletion · source_derived_draft · unverified_draft

    ### k2-different-repletion Prothrombin carboxylation normalized at 200 micrograms/day, whereas other vitamin K markers had not all returned to baseline after short repletion up to 450 micrograms/day. Condition category: nutrient_deficiency nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A liver-related marker can recover before an extrahepatic marker. organism: 21 women aged 60–80 years tissue_or_cell_type: Hepatic and extrahepatic protein markers experimental_model: Metabolic-unit dietary depletion/repletion limitations: K1 restriction probes shared vitamin K status, not an isolated dietary K2 requirement. Biochemical undercarboxylation is not equivalent to clinical bleeding or fractures. exposure: K1 restricted to 18 micrograms/day for 28 days, then stepped repletion evidence_span: {"source_cache": "artifacts/k2-research/12888638.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874", "start_char": 0, "end_char": 1461, "text_sha256": "c57beda0b2c7bdc471fd6f4bfa926e9f12846f040c95689648f599d6cceae874"} [k2-p12888638] Dietary phylloquinone depletion and repletion in older women. (2003). https://pubmed.ncbi.nlm.nih.gov/12888638/ DOI: 10.1093/jn/133.8.2565
    Complete structured claim and evidence

  3. Rat tracer experiments identified menadione derived from oral phylloquinone as a circulating precursor of tissue MK-4.

    Phylloquinone → Menadione / vitamin K3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/24085302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386", "start_char": 0, "end_char": 1653, "text_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386"}
    experimental_model
    Stable-isotope cannulation and recombinant-enzyme product analysis
    exposure
    Oral labeled phylloquinone; MS and NMR analysis
    limitations
    Rat tracing defines a precursor route; no exact human conversion fraction or advice to ingest menadione is inferred.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Rats and recombinant UBIAD1
    plain_language
    K1 and K2 metabolism connect through a precursor; they are not completely separate nutritional systems.
    primary_references
    [k2-p24085302] Menadione (vitamin K3) is a catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4 (vitamin K2) in rats. (2013). https://pubmed.ncbi.nlm.nih.gov/24085302/ DOI: 10.1074/jbc.m113.477356
    tissue_or_cell_type
    Intestine, circulation and tissue synthesis

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 175–186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stable-isotope cannulation and recombinant-enzyme product analysis · source_derived_draft · unverified_draft

    ### k2-k1-menadione Rat tracer experiments identified menadione derived from oral phylloquinone as a circulating precursor of tissue MK-4. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: K1 and K2 metabolism connect through a precursor; they are not completely separate nutritional systems. organism: Rats and recombinant UBIAD1 tissue_or_cell_type: Intestine, circulation and tissue synthesis experimental_model: Stable-isotope cannulation and recombinant-enzyme product analysis limitations: Rat tracing defines a precursor route; no exact human conversion fraction or advice to ingest menadione is inferred. exposure: Oral labeled phylloquinone; MS and NMR analysis evidence_span: {"source_cache": "artifacts/k2-research/24085302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386", "start_char": 0, "end_char": 1653, "text_sha256": "a0197882d517aa2bd4d9b2919e72c588383ad183064f1a2bf8f64f5152d28386"} [k2-p24085302] Menadione (vitamin K3) is a catabolic product of oral phylloquinone (vitamin K1) in the intestine and a circulating precursor of tissue menaquinone-4 (vitamin K2) in rats. (2013). https://pubmed.ncbi.nlm.nih.gov/24085302/ DOI: 10.1074/jbc.m113.477356
    Complete structured claim and evidence

What acts on it

  1. MK-7 showed more stable serum levels and seven- to eightfold higher accumulation during repeated intake than K1 in the comparison.

    Menaquinone-7 / MK-7 → Phylloquinone source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/17158229.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf", "start_char": 0, "end_char": 1248, "text_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf"}
    experimental_model
    Comparative human absorption and activity experiments
    exposure
    Phylloquinone versus natto-derived MK-7
    limitations
    Biochemical exposure and activity endpoints, not fracture or cardiovascular-event prevention.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Healthy volunteers
    plain_language
    Different vitamin K forms have different blood-exposure profiles.
    primary_references
    [k2-p17158229] Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. (2007). https://pubmed.ncbi.nlm.nih.gov/17158229/ DOI: 10.1182/blood-2006-08-040709
    tissue_or_cell_type
    Serum vitamers and osteocalcin

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 292–303

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparative human absorption and activity experiments · source_derived_draft · unverified_draft

    ### k2-mk7-persistence MK-7 showed more stable serum levels and seven- to eightfold higher accumulation during repeated intake than K1 in the comparison. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different vitamin K forms have different blood-exposure profiles. organism: Healthy volunteers tissue_or_cell_type: Serum vitamers and osteocalcin experimental_model: Comparative human absorption and activity experiments limitations: Biochemical exposure and activity endpoints, not fracture or cardiovascular-event prevention. exposure: Phylloquinone versus natto-derived MK-7 evidence_span: {"source_cache": "artifacts/k2-research/17158229.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf", "start_char": 0, "end_char": 1248, "text_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf"} [k2-p17158229] Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. (2007). https://pubmed.ncbi.nlm.nih.gov/17158229/ DOI: 10.1182/blood-2006-08-040709
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Cells lacking both GPX4 and FSP1 required higher K1/MK-4 concentrations to prevent ferroptosis than cells lacking GPX4 alone.

    FSP1 / AIFM2 → Menaquinone-4 / MK-4 / menatetrenone source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 16083, "end_char": 16259, "text_sha256": "942e81f7fca3a59aecc9d6cfcdc008e88931de54074e63eeb96c71af3d236eec"}
    experimental_model
    Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice
    exposure
    MK-4/K1, NAD(P)H, FSP1 loss and inhibitors
    limitations
    Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human recombinant FSP1, mammalian cells and mice
    plain_language
    The FSP1 pathway and selenium-dependent GPX4 defense are connected but not the same mechanism.
    primary_references
    [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    tissue_or_cell_type
    Lipid peroxidation and vitamin K reduction
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 812–823

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

    ### k2-fsp1-gpx4-parallel Cells lacking both GPX4 and FSP1 required higher K1/MK-4 concentrations to prevent ferroptosis than cells lacking GPX4 alone. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The FSP1 pathway and selenium-dependent GPX4 defense are connected but not the same mechanism. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 16083, "end_char": 16259, "text_sha256": "942e81f7fca3a59aecc9d6cfcdc008e88931de54074e63eeb96c71af3d236eec"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    Complete structured claim and evidence

  2. FSP1 knockout diminished MK-4 and K1 protection; wild-type FSP1 rescued protection while its myristoylation-defective G2A mutant did not.

    FSP1 / AIFM2 → Ferroptosis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 15449, "end_char": 16082, "text_sha256": "689a74e99dd668d48baef5232109dbf2898ba3adca2999a83a7bb24b321420c0"}
    experimental_model
    Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice
    exposure
    MK-4/K1, NAD(P)H, FSP1 loss and inhibitors
    limitations
    Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Human recombinant FSP1, mammalian cells and mice
    plain_language
    Providing the quinone did not fully substitute for an appropriately located working reductase.
    primary_references
    [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    tissue_or_cell_type
    Lipid peroxidation and vitamin K reduction
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 799–810

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice · source_derived_draft · unverified_draft

    ### k2-fsp1-loss FSP1 knockout diminished MK-4 and K1 protection; wild-type FSP1 rescued protection while its myristoylation-defective G2A mutant did not. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing the quinone did not fully substitute for an appropriately located working reductase. organism: Human recombinant FSP1, mammalian cells and mice tissue_or_cell_type: Lipid peroxidation and vitamin K reduction experimental_model: Enzyme/liposome chemistry, knockout cells and warfarin-exposed mice limitations: Preclinical experiments; not a demonstrated oral MK-7 treatment for ferroptosis-related disease or a self-treatment regimen for anticoagulant poisoning. exposure: MK-4/K1, NAD(P)H, FSP1 loss and inhibitors evidence_span: {"source_cache": "artifacts/k2-research/35922516.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a75e4881732cbe87173197db393b42d49fc6e8110df919fed8d63b16c9877da6", "start_char": 15449, "end_char": 16082, "text_sha256": "689a74e99dd668d48baef5232109dbf2898ba3adca2999a83a7bb24b321420c0"} [k2-p35922516] A non-canonical vitamin K cycle is a potent ferroptosis suppressor. (2022). https://pubmed.ncbi.nlm.nih.gov/35922516/ DOI: 10.1038/s41586-022-05022-3
    Complete structured claim and evidence

  3. MK-7 produced more complete osteocalcin carboxylation than the compared K1 regimen.

    Menaquinone-7 / MK-7 → Gamma-carboxylated osteocalcin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/k2-research/17158229.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf", "start_char": 0, "end_char": 1248, "text_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf"}
    experimental_model
    Comparative human absorption and activity experiments
    exposure
    Phylloquinone versus natto-derived MK-7
    limitations
    Biochemical exposure and activity endpoints, not fracture or cardiovascular-event prevention.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Healthy volunteers
    plain_language
    The biochemical modification changed; clinical bone outcomes were a separate question.
    primary_references
    [k2-p17158229] Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. (2007). https://pubmed.ncbi.nlm.nih.gov/17158229/ DOI: 10.1182/blood-2006-08-040709
    tissue_or_cell_type
    Serum vitamers and osteocalcin

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 305–316

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Comparative human absorption and activity experiments · source_derived_draft · unverified_draft

    ### k2-mk7-oc-carboxylation MK-7 produced more complete osteocalcin carboxylation than the compared K1 regimen. Condition category: normal nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The biochemical modification changed; clinical bone outcomes were a separate question. organism: Healthy volunteers tissue_or_cell_type: Serum vitamers and osteocalcin experimental_model: Comparative human absorption and activity experiments limitations: Biochemical exposure and activity endpoints, not fracture or cardiovascular-event prevention. exposure: Phylloquinone versus natto-derived MK-7 evidence_span: {"source_cache": "artifacts/k2-research/17158229.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf", "start_char": 0, "end_char": 1248, "text_sha256": "1bf2196600220143fbc5ba85e8aba71b4c8aa931f4a6c47545c3db9570283faf"} [k2-p17158229] Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. (2007). https://pubmed.ncbi.nlm.nih.gov/17158229/ DOI: 10.1182/blood-2006-08-040709
    Complete structured claim and evidence

  4. Plasma phylloquinone and percentage undercarboxylated osteocalcin did not change significantly with vitamin E supplementation despite increased PIVKA-II.

    RRR-alpha-tocopherol → Undercarboxylated osteocalcin source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men
    exposure
    RRR-alpha-tocopherol 1000 IU/day; participants were not receiving oral anticoagulant therapy.
    limitations
    Biochemical marker study, not a bleeding-events trial. The study does not identify CYP4F2 activation, direct GGCX inhibition or clinical vitamin K deficiency as the causal route.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    The vitamin K-related markers did not all respond in the same way.
    primary_references
    [e-clin-booth2004] Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status. (2004). https://pubmed.ncbi.nlm.nih.gov/15213041/ DOI: 10.1093/ajcn/80.1.143
    tissue_or_cell_type
    Circulation and vitamin K-dependent carboxylation

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1271–1282

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men · source_derived_draft · unverified_draft

    ### e-clin-vitamin-k-marker-boundary Plasma phylloquinone and percentage undercarboxylated osteocalcin did not change significantly with vitamin E supplementation despite increased PIVKA-II. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The vitamin K-related markers did not all respond in the same way. organism: Homo sapiens tissue_or_cell_type: Circulation and vitamin K-dependent carboxylation experimental_model: Two independent 12-week randomized trials; 38 adults with rheumatoid arthritis and 32 healthy men limitations: Biochemical marker study, not a bleeding-events trial. The study does not identify CYP4F2 activation, direct GGCX inhibition or clinical vitamin K deficiency as the causal route. exposure: RRR-alpha-tocopherol 1000 IU/day; participants were not receiving oral anticoagulant therapy. cross_nutrient: true [e-clin-booth2004] Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status. (2004). https://pubmed.ncbi.nlm.nih.gov/15213041/ DOI: 10.1093/ajcn/80.1.143
    Complete structured claim and evidence

  5. Alpha-tocopherol did not increase phylloquinone omega-hydroxylation in CYP4F2 microsomes; the study reported a slight decrease in apparent phylloquinone Vmax.

    RRR-alpha-tocopherol → CYP4F2-mediated phylloquinone omega-hydroxylation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Recombinant human CYP4F2 co-substrate kinetics
    exposure
    Labeled phylloquinone 0–50 µM with RRR-alpha-tocopherol 0–50 µM or SRR-alpha-tocopherol 0–100 µM; 30 min, 37 °C, 1 mM NADPH.
    limitations
    Does not exclude other mechanisms of vitamin E–K interaction in animals or humans.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Human protein in insect microsomes
    plain_language
    This assay did not support faster vitamin K1 breakdown caused by alpha-tocopherol.
    primary_references
    [farley2013] ω-Hydroxylation of phylloquinone by CYP4F2 is not increased by α-tocopherol. (2013). https://pubmed.ncbi.nlm.nih.gov/23650179/ DOI: 10.1002/mnfr.201200797
    tissue_or_cell_type
    Microsomal enzyme preparation

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 467–478

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human CYP4F2 co-substrate kinetics · source_derived_draft · unverified_draft

    ### ve-transport-alpha-does-not-activate-k1-catabolism Alpha-tocopherol did not increase phylloquinone omega-hydroxylation in CYP4F2 microsomes; the study reported a slight decrease in apparent phylloquinone Vmax. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: This assay did not support faster vitamin K1 breakdown caused by alpha-tocopherol. organism: Human protein in insect microsomes tissue_or_cell_type: Microsomal enzyme preparation experimental_model: Recombinant human CYP4F2 co-substrate kinetics limitations: Does not exclude other mechanisms of vitamin E–K interaction in animals or humans. exposure: Labeled phylloquinone 0–50 µM with RRR-alpha-tocopherol 0–50 µM or SRR-alpha-tocopherol 0–100 µM; 30 min, 37 °C, 1 mM NADPH. cross_nutrient: true [farley2013] ω-Hydroxylation of phylloquinone by CYP4F2 is not increased by α-tocopherol. (2013). https://pubmed.ncbi.nlm.nih.gov/23650179/ DOI: 10.1002/mnfr.201200797
    Complete structured claim and evidence

  6. Human CYP4F2-expressing microsomes hydroxylated phylloquinone, demonstrating substrate overlap with tocopherol catabolism.

    Human cytochrome P450 4F2 → Omega-hydroxyphylloquinone source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Recombinant CYP4F2 kinetic assay
    exposure
    25 pmol CYP4F2; labeled phylloquinone 1–100 µM; 1 mM NADPH; 30 min at 37 °C.
    limitations
    Shared substrate use alone does not imply vitamin E accelerates vitamin K depletion.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Human protein in insect microsomes
    plain_language
    Vitamins E and K1 share an initial catabolic enzyme.
    primary_references
    [farley2013] ω-Hydroxylation of phylloquinone by CYP4F2 is not increased by α-tocopherol. (2013). https://pubmed.ncbi.nlm.nih.gov/23650179/ DOI: 10.1002/mnfr.201200797
    tissue_or_cell_type
    Microsomal enzyme preparation

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 454–465

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant CYP4F2 kinetic assay · source_derived_draft · unverified_draft

    ### ve-transport-cyp4f2-k1-hydroxylation Human CYP4F2-expressing microsomes hydroxylated phylloquinone, demonstrating substrate overlap with tocopherol catabolism. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamins E and K1 share an initial catabolic enzyme. organism: Human protein in insect microsomes tissue_or_cell_type: Microsomal enzyme preparation experimental_model: Recombinant CYP4F2 kinetic assay limitations: Shared substrate use alone does not imply vitamin E accelerates vitamin K depletion. exposure: 25 pmol CYP4F2; labeled phylloquinone 1–100 µM; 1 mM NADPH; 30 min at 37 °C. cross_nutrient: true [farley2013] ω-Hydroxylation of phylloquinone by CYP4F2 is not increased by α-tocopherol. (2013). https://pubmed.ncbi.nlm.nih.gov/23650179/ DOI: 10.1002/mnfr.201200797
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards