Component

Sensory neuropathy

Independently recorded entity or measured process. Linked claims specify compartment, assay and experimental scope.

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. All five volunteers developed sensory symptoms and quantitative sensory abnormalities; the 3 g/day group became symptomatic sooner than the 1 g/day group.

    Pyridoxine → Sensory neuropathy source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    Experimental excess, not nutrient deficiency
    experimental_model
    Five healthy volunteers prospectively followed during experimental pyridoxine excess.
    exposure
    Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures.
    limitations
    Five volunteers at gram doses; cannot determine a lowest toxic dose, safe upper intake or equivalence of different B6 forms.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    At very high exposure, more pyridoxine produced earlier sensory toxicity.
    primary_references
    [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    tissue_or_cell_type
    Peripheral sensory function

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1559–1570

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five healthy volunteers prospectively followed during experimental pyridoxine excess. · source_derived_draft · unverified_draft

    ### b6-pyridoxine-dose-latency All five volunteers developed sensory symptoms and quantitative sensory abnormalities; the 3 g/day group became symptomatic sooner than the 1 g/day group. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: At very high exposure, more pyridoxine produced earlier sensory toxicity. organism: Homo sapiens tissue_or_cell_type: Peripheral sensory function experimental_model: Five healthy volunteers prospectively followed during experimental pyridoxine excess. limitations: Five volunteers at gram doses; cannot determine a lowest toxic dose, safe upper intake or equivalence of different B6 forms. exposure: Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures. availability_state: Experimental excess, not nutrient deficiency [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    Complete structured claim and evidence

  2. After long-term 1250–1750 mg/day exposure, the reported patient recovered sensory function and nerve potentials following reduction to 500 mg/day.

    Pyridoxine → Sensory neuropathy source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Single patient with homocystinuria and long-term high-dose pyridoxine exposure.
    exposure
    1250–1750 mg/day for 20 years; subsequently reduced to 500 mg/day. Case history, not evidence that the reduced dose is safe generally.
    limitations
    Single homocystinuria case; does not establish universal reversibility or safety of 500 mg/day. The article background statement about 50 mg is not treated as an experimentally determined threshold.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    Recovery was possible in this individual despite long exposure.
    primary_references
    [b6-echanizlaguna2018] Regressive pyridoxine-induced sensory neuronopathy in a patient with homocystinuria (2018). https://pubmed.ncbi.nlm.nih.gov/29954767/ DOI: 10.1136/bcr-2018-225059
    tissue_or_cell_type
    Peripheral sensory nerves

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1596–1606

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single patient with homocystinuria and long-term high-dose pyridoxine exposure. · source_derived_draft · unverified_draft

    ### b6-toxicity-case-recovery After long-term 1250–1750 mg/day exposure, the reported patient recovered sensory function and nerve potentials following reduction to 500 mg/day. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Recovery was possible in this individual despite long exposure. organism: Homo sapiens tissue_or_cell_type: Peripheral sensory nerves experimental_model: Single patient with homocystinuria and long-term high-dose pyridoxine exposure. limitations: Single homocystinuria case; does not establish universal reversibility or safety of 500 mg/day. The article background statement about 50 mg is not treated as an experimentally determined threshold. exposure: 1250–1750 mg/day for 20 years; subsequently reduced to 500 mg/day. Case history, not evidence that the reduced dose is safe generally. [b6-echanizlaguna2018] Regressive pyridoxine-induced sensory neuronopathy in a patient with homocystinuria (2018). https://pubmed.ncbi.nlm.nih.gov/29954767/ DOI: 10.1136/bcr-2018-225059
    Complete structured claim and evidence

  3. Symptoms progressed for two to three weeks after pyridoxine withdrawal despite normalized serum PLP.

    Pyridoxine → Sensory neuropathy source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Five healthy volunteers prospectively followed during experimental pyridoxine excess.
    exposure
    Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures.
    limitations
    Demonstrates clinical timing; does not identify the molecular injury mechanism or prove irreversible damage.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    A blood vitamin level returned to normal before the nerve symptoms stopped worsening.
    primary_references
    [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    tissue_or_cell_type
    Peripheral sensory function after exposure withdrawal

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1584–1594

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five healthy volunteers prospectively followed during experimental pyridoxine excess. · source_derived_draft · unverified_draft

    ### b6-toxicity-coasting Symptoms progressed for two to three weeks after pyridoxine withdrawal despite normalized serum PLP. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A blood vitamin level returned to normal before the nerve symptoms stopped worsening. organism: Homo sapiens tissue_or_cell_type: Peripheral sensory function after exposure withdrawal experimental_model: Five healthy volunteers prospectively followed during experimental pyridoxine excess. limitations: Demonstrates clinical timing; does not identify the molecular injury mechanism or prove irreversible damage. exposure: Pyridoxine 1 or 3 g/day, stopped with clinical/laboratory abnormality; very high historical exposures. [b6-berger1992] Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity (1992). https://pubmed.ncbi.nlm.nih.gov/1620347/ DOI: 10.1212/wnl.42.7.1367
    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.

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