Component

Intestinal permeability to macromolecules

Intestinal permeability to macromolecules. Species, exposure and limitations are retained in each linked claim.

4 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. Intestinal permeability and gut bacterial dysbiosis were associated with behavioural markers of alcohol-dependence severity.

    Intestinal permeability to macromolecules → Alcohol craving and dependence severity source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/25288760.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b62793e216036689dd924357291c4512c5e9bcf7e7b41429e6bb72b2022f6a6c", "start_char": 0, "end_char": 1345, "text_sha256": "b62793e216036689dd924357291c4512c5e9bcf7e7b41429e6bb72b2022f6a6c"}
    experimental_model
    Alcohol-dependent patients with permeability, microbiome and behavioural measures
    exposure
    Alcohol dependence with detoxification
    limitations
    Links the gut measurements to craving. It is an association in a dependent population, and the direction of causation is not established.
    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
    How leaky the gut is tracks with how severe the dependence is.
    primary_references
    [alcohol-p25288760] Intestinal permeability, gut-bacterial dysbiosis, and behavioral markers of alcohol-dependence severity. (2014). https://pubmed.ncbi.nlm.nih.gov/25288760/ DOI: 10.1073/pnas.1415174111
    tissue_or_cell_type
    Intestine and behaviour

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 488–499

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Alcohol-dependent patients with permeability, microbiome and behavioural measures · source_derived_draft · unverified_draft

    ### alcohol-permeability-craving Intestinal permeability and gut bacterial dysbiosis were associated with behavioural markers of alcohol-dependence severity. Condition category: normal 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: How leaky the gut is tracks with how severe the dependence is. organism: Human tissue_or_cell_type: Intestine and behaviour experimental_model: Alcohol-dependent patients with permeability, microbiome and behavioural measures limitations: Links the gut measurements to craving. It is an association in a dependent population, and the direction of causation is not established. exposure: Alcohol dependence with detoxification evidence_span: {"source_cache": "artifacts/alcohol-research/25288760.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b62793e216036689dd924357291c4512c5e9bcf7e7b41429e6bb72b2022f6a6c", "start_char": 0, "end_char": 1345, "text_sha256": "b62793e216036689dd924357291c4512c5e9bcf7e7b41429e6bb72b2022f6a6c"} [alcohol-p25288760] Intestinal permeability, gut-bacterial dysbiosis, and behavioral markers of alcohol-dependence severity. (2014). https://pubmed.ncbi.nlm.nih.gov/25288760/ DOI: 10.1073/pnas.1415174111
    Complete structured claim and evidence

What acts on it

  1. Fructose promoted leaky gut, endotoxaemia and liver fibrosis through ethanol-inducible cytochrome P450-2E1-mediated oxidative and nitrative stress.

    Human cytochrome P450 2E1 → Intestinal permeability to macromolecules source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/30959577.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d", "start_char": 0, "end_char": 1961, "text_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d"}
    experimental_model
    Fructose feeding in mice with CYP2E1 deletion and gut barrier measurement
    exposure
    Fructose feeding with and without CYP2E1
    limitations
    Recorded because it isolates the enzyme: the leak and fibrosis required CYP2E1, which ethanol induces. The driver here is fructose, not ethanol.
    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
    Mouse
    plain_language
    The enzyme alcohol stabilises is itself enough to open the gut barrier.
    primary_references
    [alcohol-p30959577] Fructose Promotes Leaky Gut, Endotoxemia, and Liver Fibrosis Through Ethanol-Inducible Cytochrome P450-2E1-Mediated Oxidative and Nitrative Stress. (2021). https://pubmed.ncbi.nlm.nih.gov/30959577/ DOI: 10.1002/hep.30652
    tissue_or_cell_type
    Intestine and liver

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 501–512

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fructose feeding in mice with CYP2E1 deletion and gut barrier measurement · source_derived_draft · unverified_draft

    ### alcohol-cyp2e1-leaky-gut Fructose promoted leaky gut, endotoxaemia and liver fibrosis through ethanol-inducible cytochrome P450-2E1-mediated oxidative and nitrative stress. Condition category: normal 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 enzyme alcohol stabilises is itself enough to open the gut barrier. organism: Mouse tissue_or_cell_type: Intestine and liver experimental_model: Fructose feeding in mice with CYP2E1 deletion and gut barrier measurement limitations: Recorded because it isolates the enzyme: the leak and fibrosis required CYP2E1, which ethanol induces. The driver here is fructose, not ethanol. exposure: Fructose feeding with and without CYP2E1 evidence_span: {"source_cache": "artifacts/alcohol-research/30959577.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d", "start_char": 0, "end_char": 1961, "text_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d"} [alcohol-p30959577] Fructose Promotes Leaky Gut, Endotoxemia, and Liver Fibrosis Through Ethanol-Inducible Cytochrome P450-2E1-Mediated Oxidative and Nitrative Stress. (2021). https://pubmed.ncbi.nlm.nih.gov/30959577/ DOI: 10.1002/hep.30652
    Complete structured claim and evidence

  2. Patients with chronic alcohol abuse showed increased intestinal permeability to macromolecules and endotoxaemia, varying across stages of alcohol-induced liver disease.

    Habitual alcohol consumption → Intestinal permeability to macromolecules source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/10845660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0342f8e351dde29e075eaf2d1920f26d1e8ef9d9a704947dc6c08f6f5fde846d", "start_char": 0, "end_char": 1618, "text_sha256": "0342f8e351dde29e075eaf2d1920f26d1e8ef9d9a704947dc6c08f6f5fde846d"}
    experimental_model
    Intestinal permeability and endotoxin measurement across stages of alcohol-induced liver disease
    exposure
    Chronic alcohol abuse, staged by liver disease severity
    limitations
    Human observational staging. It shows permeability tracks disease stage; it cannot establish which came first.
    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
    The gut wall leaks and bacterial fragments reach the blood.
    primary_references
    [alcohol-p10845660] Increased intestinal permeability to macromolecules and endotoxemia in patients with chronic alcohol abuse in different stages of alcohol-induced liver disease. (2000). https://pubmed.ncbi.nlm.nih.gov/10845660/ DOI: 10.1016/s0168-8278(00)80242-1
    tissue_or_cell_type
    Intestine and blood

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 462–473

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal permeability and endotoxin measurement across stages of alcohol-induced liver disease · source_derived_draft · unverified_draft

    ### alcohol-permeability-endotoxin Patients with chronic alcohol abuse showed increased intestinal permeability to macromolecules and endotoxaemia, varying across stages of alcohol-induced liver disease. Condition category: normal 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 gut wall leaks and bacterial fragments reach the blood. organism: Human tissue_or_cell_type: Intestine and blood experimental_model: Intestinal permeability and endotoxin measurement across stages of alcohol-induced liver disease limitations: Human observational staging. It shows permeability tracks disease stage; it cannot establish which came first. exposure: Chronic alcohol abuse, staged by liver disease severity evidence_span: {"source_cache": "artifacts/alcohol-research/10845660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0342f8e351dde29e075eaf2d1920f26d1e8ef9d9a704947dc6c08f6f5fde846d", "start_char": 0, "end_char": 1618, "text_sha256": "0342f8e351dde29e075eaf2d1920f26d1e8ef9d9a704947dc6c08f6f5fde846d"} [alcohol-p10845660] Increased intestinal permeability to macromolecules and endotoxemia in patients with chronic alcohol abuse in different stages of alcohol-induced liver disease. (2000). https://pubmed.ncbi.nlm.nih.gov/10845660/ DOI: 10.1016/s0168-8278(00)80242-1
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Alcohol exposure significantly reduced the ileal zinc concentration in association with accumulation of reactive oxygen species, and significantly increased permeability of the ileum without affecting the duodenum or jejunum.

    Ethanol → Ileal tissue zinc concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/20167873.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e", "start_char": 0, "end_char": 1542, "text_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e"}
    experimental_model
    Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation
    exposure
    Four weeks of alcohol liquid diet; zinc deprivation in culture
    limitations
    The regional specificity and the separate zinc-deprivation arm are what make the nutrient claim interpretable. The exaggeration experiment is in cultured cells.
    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
    Mouse
    plain_language
    Alcohol drains zinc from one specific stretch of gut, and that is exactly where it leaks.
    primary_references
    [alcohol-p20167873] The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. (2010). https://pubmed.ncbi.nlm.nih.gov/20167873/ DOI: 10.1152/ajpgi.00350.2009
    tissue_or_cell_type
    Ileum and Caco-2 monolayers
    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 761–772

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation · source_derived_draft · unverified_draft

    ### alcohol-alcohol-ileal-zinc Alcohol exposure significantly reduced the ileal zinc concentration in association with accumulation of reactive oxygen species, and significantly increased permeability of the ileum without affecting the duodenum or jejunum. 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: Alcohol drains zinc from one specific stretch of gut, and that is exactly where it leaks. organism: Mouse tissue_or_cell_type: Ileum and Caco-2 monolayers experimental_model: Pair-fed alcohol mice with regional permeability measurement and Caco-2 zinc deprivation limitations: The regional specificity and the separate zinc-deprivation arm are what make the nutrient claim interpretable. The exaggeration experiment is in cultured cells. exposure: Four weeks of alcohol liquid diet; zinc deprivation in culture evidence_span: {"source_cache": "artifacts/alcohol-research/20167873.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e", "start_char": 0, "end_char": 1542, "text_sha256": "12b4bf025e28831a9d613fd7d6b62275f573f8a8999efb73d763bb8e8059b15e"} [alcohol-p20167873] The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. (2010). https://pubmed.ncbi.nlm.nih.gov/20167873/ DOI: 10.1152/ajpgi.00350.2009
    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