Component

Thiamine deficiency

Thiamine deficiency. 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 it acts on

  1. Interaction of thiamine deficiency and voluntary alcohol consumption disrupted rat corpus callosum ultrastructure.

    Thiamine deficiency → Corpus callosum ultrastructure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/17299515.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e691ddc58fc07fe2716bf42e4cc6a65eed1b59ebc3696a28749459c7c27e4772", "start_char": 0, "end_char": 2513, "text_sha256": "e691ddc58fc07fe2716bf42e4cc6a65eed1b59ebc3696a28749459c7c27e4772"}
    experimental_model
    Rats given voluntary alcohol with and without induced thiamine deficiency, with electron microscopy
    exposure
    Voluntary alcohol consumption combined with thiamine deficiency
    limitations
    A controlled factorial animal experiment, which is what an observational human series cannot provide.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Rat
    plain_language
    In a controlled experiment the combination damaged the bridge between the brain hemispheres.
    primary_references
    [alcohol-p17299515] Interaction of thiamine deficiency and voluntary alcohol consumption disrupts rat corpus callosum ultrastructure. (2007). https://pubmed.ncbi.nlm.nih.gov/17299515/ DOI: 10.1038/sj.npp.1301332
    tissue_or_cell_type
    Corpus callosum
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 735–746

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats given voluntary alcohol with and without induced thiamine deficiency, with electron microscopy · source_derived_draft · unverified_draft

    ### alcohol-corpus-callosum Interaction of thiamine deficiency and voluntary alcohol consumption disrupted rat corpus callosum ultrastructure. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: In a controlled experiment the combination damaged the bridge between the brain hemispheres. organism: Rat tissue_or_cell_type: Corpus callosum experimental_model: Rats given voluntary alcohol with and without induced thiamine deficiency, with electron microscopy limitations: A controlled factorial animal experiment, which is what an observational human series cannot provide. exposure: Voluntary alcohol consumption combined with thiamine deficiency evidence_span: {"source_cache": "artifacts/alcohol-research/17299515.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e691ddc58fc07fe2716bf42e4cc6a65eed1b59ebc3696a28749459c7c27e4772", "start_char": 0, "end_char": 2513, "text_sha256": "e691ddc58fc07fe2716bf42e4cc6a65eed1b59ebc3696a28749459c7c27e4772"} [alcohol-p17299515] Interaction of thiamine deficiency and voluntary alcohol consumption disrupts rat corpus callosum ultrastructure. (2007). https://pubmed.ncbi.nlm.nih.gov/17299515/ DOI: 10.1038/sj.npp.1301332
    Complete structured claim and evidence

  2. Thiamine deficiency impairs oxidative metabolic pathways and contributes to ethanol-induced neurotoxicity, with poor nutrition contributing to the alcoholic syndrome.

    Thiamine deficiency → Transketolase activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/28225048.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6", "start_char": 0, "end_char": 1824, "text_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6"}
    experimental_model
    Review of thiamine deficiency and oxidative metabolic pathways in ethanol neurotoxicity
    exposure
    Chronic alcohol use with poor nutrition
    limitations
    A review, labelled as such, linking the coenzyme role to the clinical syndrome. Marchiafava-Bignami disease is rare, so the clinical anchor is narrow.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Human
    plain_language
    Without the coenzyme the pathways that burn sugar for the brain stall.
    primary_references
    [alcohol-p28225048] Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity: how poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. (2017). https://pubmed.ncbi.nlm.nih.gov/28225048/ DOI: 10.1038/ejcn.2016.267
    tissue_or_cell_type
    Brain
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 748–759

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of thiamine deficiency and oxidative metabolic pathways in ethanol neurotoxicity · source_derived_draft · unverified_draft

    ### alcohol-thiamine-oxidative-pathways Thiamine deficiency impairs oxidative metabolic pathways and contributes to ethanol-induced neurotoxicity, with poor nutrition contributing to the alcoholic syndrome. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Without the coenzyme the pathways that burn sugar for the brain stall. organism: Human tissue_or_cell_type: Brain experimental_model: Review of thiamine deficiency and oxidative metabolic pathways in ethanol neurotoxicity limitations: A review, labelled as such, linking the coenzyme role to the clinical syndrome. Marchiafava-Bignami disease is rare, so the clinical anchor is narrow. exposure: Chronic alcohol use with poor nutrition evidence_span: {"source_cache": "artifacts/alcohol-research/28225048.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6", "start_char": 0, "end_char": 1824, "text_sha256": "14985f03480c03e14fe75f00e454323cd6f5d414f3775e5ee0d4d4da7825e8c6"} [alcohol-p28225048] Thiamine deficiency, oxidative metabolic pathways and ethanol-induced neurotoxicity: how poor nutrition contributes to the alcoholic syndrome, as Marchiafava-Bignami disease. (2017). https://pubmed.ncbi.nlm.nih.gov/28225048/ DOI: 10.1038/ejcn.2016.267
    Complete structured claim and evidence

  3. The pathophysiology of alcoholic brain damage involves synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease.

    Thiamine deficiency → Alcoholic brain damage source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/7596324.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30469341e3044e901ef2ebfa2e84bfb83b48044a455f1f0e415662eb2a9c6368", "start_char": 0, "end_char": 1186, "text_sha256": "30469341e3044e901ef2ebfa2e84bfb83b48044a455f1f0e415662eb2a9c6368"}
    experimental_model
    Review of alcoholic brain damage separating ethanol, thiamine deficiency and liver disease
    exposure
    Chronic alcohol exposure with and without thiamine deficiency
    limitations
    A review, labelled as such. Its value here is that it insists the three causes be separated rather than merged into one syndrome.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Human and animal
    plain_language
    The drinking and the missing vitamin do more damage together than either does alone.
    primary_references
    [alcohol-p7596324] Pathophysiology of alcoholic brain damage: synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease. (1995). https://pubmed.ncbi.nlm.nih.gov/7596324/ DOI: 10.1007/bf01991777
    tissue_or_cell_type
    Brain
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 722–733

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Review of alcoholic brain damage separating ethanol, thiamine deficiency and liver disease · source_derived_draft · unverified_draft

    ### alcohol-thiamine-synergy The pathophysiology of alcoholic brain damage involves synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease. Condition category: nutrient_deficiency nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The drinking and the missing vitamin do more damage together than either does alone. organism: Human and animal tissue_or_cell_type: Brain experimental_model: Review of alcoholic brain damage separating ethanol, thiamine deficiency and liver disease limitations: A review, labelled as such. Its value here is that it insists the three causes be separated rather than merged into one syndrome. exposure: Chronic alcohol exposure with and without thiamine deficiency evidence_span: {"source_cache": "artifacts/alcohol-research/7596324.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30469341e3044e901ef2ebfa2e84bfb83b48044a455f1f0e415662eb2a9c6368", "start_char": 0, "end_char": 1186, "text_sha256": "30469341e3044e901ef2ebfa2e84bfb83b48044a455f1f0e415662eb2a9c6368"} [alcohol-p7596324] Pathophysiology of alcoholic brain damage: synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease. (1995). https://pubmed.ncbi.nlm.nih.gov/7596324/ DOI: 10.1007/bf01991777
    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