Component

Hemorrhage

Hemorrhage. Species, exposure and limitations are retained in each linked claim.

3 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 acts on it

  1. A patient taking aspirin for secondary stroke prevention had an acute cerebellar hemorrhage after seven consecutive days of nattokinase at 400 mg daily, with multiple cerebral microbleeds on MRI.

    Commercial nattokinase supplement, composition study-specific → Hemorrhage source_derived_draftungraded
    Experimental context and source evidence
    duration
    7 days
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    experimental_model
    Human (single case report)
    exposure
    Nattokinase 400 mg daily with concurrent aspirin
    limitations
    One case with strong predispositions, so neither causality nor incidence can be inferred from it. It is recorded because formal pharmacokinetic and pharmacodynamic interaction studies with warfarin, direct oral anticoagulants, aspirin or clopidogrel are absent from everything read here, and because the human aPTT and closure-time findings make an additive effect plausible.
    organism
    Human (single case report)
    plain_language
    A patient taking aspirin for secondary stroke prevention had an acute cerebellar hemorrhage after seven consecutive days of nattokinase at 400 mg daily, with multiple cerebral microbleeds on MRI.
    primary_references
    Cerebellar hemorrhage provoked by combined use of nattokinase and aspirin in a patient with cerebral microbleeds. (2008) https://pubmed.ncbi.nlm.nih.gov/18310985/ DOI: 10.2169/internalmedicine.47.0620
    route
    In vivo, oral
    tissue
    Cerebellum, with cerebral microbleeds on MR imaging

    Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 1390–1390

    Original AI-assisted curation built from a supplied entity-first document of 105 entities and 129 claims. Every reference in that document was resolved against live PubMed with its abstract read and its DOI cross-checked on 2026-09-23, and the EFSA novel-food opinion was retrieved and read in full. That check corrected two PMIDs that pointed at unrelated papers, two DOIs, and two papers recorded as carrying no erratum that do carry one; it also reversed three findings the supplied document had stated backwards. Two papers carry a published correction, recorded as such and not as a retraction. Three sources are not indexed in PubMed and are cited by what they have. Laboratory lineages are recorded, so the four papers from one group, the three from another and the two readings of a single applicant dossier cannot be counted as separate lines of support. Study-specific doses, units, populations and limitations retained; activity units are never converted between systems. Not publisher full text. · supports · Human (single case report) · source_derived_draft · unverified_draft

    A patient taking aspirin for secondary stroke prevention had an acute cerebellar hemorrhage after seven consecutive days of nattokinase at 400 mg daily, with multiple cerebral microbleeds on MRI.
    Complete structured claim and evidence

  2. Vkorc1-null mice died 2–20 days after birth with severe deficiency of carboxylated clotting factors and extensive hemorrhage.

    Mouse vitamin K epoxide reductase / Vkorc1 → Hemorrhage source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/19492146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c", "start_char": 0, "end_char": 1237, "text_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c"}
    experimental_model
    Knockout and oral vitamin K rescue
    exposure
    Vkorc1 deletion
    limitations
    Shared vitamin K pathway; the rescue is not proof that K2 supplements replace medical management. Later alternative reductase findings prevent treating the paper as evidence that no bypass can exist.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Mice
    plain_language
    A major failure in the shared vitamin K cycle can become a clotting failure.
    primary_references
    [k2-p19492146] VKORC1 deficiency in mice causes early postnatal lethality due to severe bleeding. (2009). https://pubmed.ncbi.nlm.nih.gov/19492146/ DOI: 10.1160/th09-03-0204
    tissue_or_cell_type
    Postnatal coagulation and skeletal development
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 903–914

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Knockout and oral vitamin K rescue · source_derived_draft · unverified_draft

    ### k2-vkor-bleeding Vkorc1-null mice died 2–20 days after birth with severe deficiency of carboxylated clotting factors and extensive hemorrhage. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A major failure in the shared vitamin K cycle can become a clotting failure. organism: Mice tissue_or_cell_type: Postnatal coagulation and skeletal development experimental_model: Knockout and oral vitamin K rescue limitations: Shared vitamin K pathway; the rescue is not proof that K2 supplements replace medical management. Later alternative reductase findings prevent treating the paper as evidence that no bypass can exist. exposure: Vkorc1 deletion evidence_span: {"source_cache": "artifacts/k2-research/19492146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c", "start_char": 0, "end_char": 1237, "text_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c"} [k2-p19492146] VKORC1 deficiency in mice causes early postnatal lethality due to severe bleeding. (2009). https://pubmed.ncbi.nlm.nih.gov/19492146/ DOI: 10.1160/th09-03-0204
    Complete structured claim and evidence

  3. Oral vitamin K rescued the lethal bleeding phenotype of Vkorc1-null mice.

    Vitamin K → Hemorrhage source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/k2-research/19492146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c", "start_char": 0, "end_char": 1237, "text_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c"}
    experimental_model
    Knockout and oral vitamin K rescue
    exposure
    Vkorc1 deletion
    limitations
    Shared vitamin K pathway; the rescue is not proof that K2 supplements replace medical management. Later alternative reductase findings prevent treating the paper as evidence that no bypass can exist.
    nutrient_topic
    Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin K2 / menaquinone family
    organism
    Mice
    plain_language
    Cofactor supply could bypass enough of the defect in this experimental model.
    primary_references
    [k2-p19492146] VKORC1 deficiency in mice causes early postnatal lethality due to severe bleeding. (2009). https://pubmed.ncbi.nlm.nih.gov/19492146/ DOI: 10.1160/th09-03-0204
    tissue_or_cell_type
    Postnatal coagulation and skeletal development
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin K2: menaquinone forms, carboxylation, recycling and nutrient interactions (2026-09-17) · lines 916–927

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Knockout and oral vitamin K rescue · source_derived_draft · unverified_draft

    ### k2-vkor-rescue Oral vitamin K rescued the lethal bleeding phenotype of Vkorc1-null mice. Condition category: machinery_impairment nutrient_topic: Vitamin K2 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cofactor supply could bypass enough of the defect in this experimental model. organism: Mice tissue_or_cell_type: Postnatal coagulation and skeletal development experimental_model: Knockout and oral vitamin K rescue limitations: Shared vitamin K pathway; the rescue is not proof that K2 supplements replace medical management. Later alternative reductase findings prevent treating the paper as evidence that no bypass can exist. exposure: Vkorc1 deletion evidence_span: {"source_cache": "artifacts/k2-research/19492146.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c", "start_char": 0, "end_char": 1237, "text_sha256": "4f3957681861ebb8860b46b4a29e6b9c142ba79e7abff1af925dd48b7f0e0c6c"} [k2-p19492146] VKORC1 deficiency in mice causes early postnatal lethality due to severe bleeding. (2009). https://pubmed.ncbi.nlm.nih.gov/19492146/ DOI: 10.1160/th09-03-0204
    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