Component

Habitual alcohol consumption

Habitual alcohol consumption. Species, exposure and limitations are retained in each linked claim.

9 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. Hepatic zinc content differed across stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis.

    Habitual alcohol consumption → Hepatic zinc content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/3192174.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3", "start_char": 0, "end_char": 1588, "text_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3"}
    experimental_model
    Hepatic zinc measurement across stages of alcoholic liver disease and chronic hepatitis
    exposure
    Staged alcoholic liver disease compared with chronic hepatitis
    limitations
    A human tissue measurement with a disease control group, which separates alcohol from liver disease in general.
    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 liver itself holds less zinc as the disease advances.
    primary_references
    [alcohol-p3192174] Hepatic zinc content in patients with various stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis. (1988). https://pubmed.ncbi.nlm.nih.gov/3192174/ DOI: 10.1002/hep.1840080622
    tissue_or_cell_type
    Liver
    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 800–811

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hepatic zinc measurement across stages of alcoholic liver disease and chronic hepatitis · source_derived_draft · unverified_draft

    ### alcohol-hepatic-zinc-depletion Hepatic zinc content differed across stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis. 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 liver itself holds less zinc as the disease advances. organism: Human tissue_or_cell_type: Liver experimental_model: Hepatic zinc measurement across stages of alcoholic liver disease and chronic hepatitis limitations: A human tissue measurement with a disease control group, which separates alcohol from liver disease in general. exposure: Staged alcoholic liver disease compared with chronic hepatitis evidence_span: {"source_cache": "artifacts/alcohol-research/3192174.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3", "start_char": 0, "end_char": 1588, "text_sha256": "7f6eab91e632a1ddf96193486fc1be8bffa4acb0b48d062fef2b65affe168ca3"} [alcohol-p3192174] Hepatic zinc content in patients with various stages of alcoholic liver disease and in patients with chronic active and chronic persistent hepatitis. (1988). https://pubmed.ncbi.nlm.nih.gov/3192174/ DOI: 10.1002/hep.1840080622
    Complete structured claim and evidence

  2. In unadjusted models, protective effects were identified for alcohol consumption against all-cause mortality in pooled English cohorts of adults aged 50 and over, which the authors examine to test the suitability of age-specific limits.

    Habitual alcohol consumption → All-cause mortality source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/25670624.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2915b9b52e02cedee89d34376f15e2efc97c6a66e83377240892b305c0c5c1b8", "start_char": 0, "end_char": 3171, "text_sha256": "2915b9b52e02cedee89d34376f15e2efc97c6a66e83377240892b305c0c5c1b8"}
    experimental_model
    Pooled analysis of up to 10 population cohorts from the Health Survey for England
    exposure
    Self-reported weekly and heaviest-day consumption in adults aged 50 and over
    limitations
    A large observational cohort with the abstainer comparison the reanalysis above criticises. Protective effects were identified in unadjusted models.
    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
    In the raw numbers, older people who drank moderately died less often.
    primary_references
    [alcohol-p25670624] All cause mortality and the case for age specific alcohol consumption guidelines: pooled analyses of up to 10 population based cohorts. (2015). https://pubmed.ncbi.nlm.nih.gov/25670624/ DOI: 10.1136/bmj.h384
    tissue_or_cell_type
    Whole body

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 592–603

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pooled analysis of up to 10 population cohorts from the Health Survey for England · source_derived_draft · unverified_draft

    ### alcohol-jcurve-observed In unadjusted models, protective effects were identified for alcohol consumption against all-cause mortality in pooled English cohorts of adults aged 50 and over, which the authors examine to test the suitability of age-specific limits. 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: In the raw numbers, older people who drank moderately died less often. organism: Human tissue_or_cell_type: Whole body experimental_model: Pooled analysis of up to 10 population cohorts from the Health Survey for England limitations: A large observational cohort with the abstainer comparison the reanalysis above criticises. Protective effects were identified in unadjusted models. exposure: Self-reported weekly and heaviest-day consumption in adults aged 50 and over evidence_span: {"source_cache": "artifacts/alcohol-research/25670624.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2915b9b52e02cedee89d34376f15e2efc97c6a66e83377240892b305c0c5c1b8", "start_char": 0, "end_char": 3171, "text_sha256": "2915b9b52e02cedee89d34376f15e2efc97c6a66e83377240892b305c0c5c1b8"} [alcohol-p25670624] All cause mortality and the case for age specific alcohol consumption guidelines: pooled analyses of up to 10 population based cohorts. (2015). https://pubmed.ncbi.nlm.nih.gov/25670624/ DOI: 10.1136/bmj.h384
    Complete structured claim and evidence

  3. Thirty-five of 66 alcoholic subjects selected for normal liver function and haematology had plasma PLP below 5 ng/ml, the lowest value found in 94 controls.

    Habitual alcohol consumption → Plasma pyridoxal 5-prime-phosphate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/4359937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08", "start_char": 0, "end_char": 1650, "text_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08"}
    experimental_model
    Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays
    exposure
    Chronic alcohol abuse; acetaldehyde and ethanol applied to erythrocytes
    limitations
    Selecting subjects without abnormal liver function isolates the vitamin effect from liver disease. The phosphatase mechanism is shown in erythrocytes, not liver.
    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
    More than half had less of the active vitamin than any healthy control, with healthy livers.
    primary_references
    [alcohol-p4359937] Vitamin B6 metabolism in chronic alcohol abuse. Pyridoxal phosphate levels in plasma and the effects of acetaldehyde on pyridoxal phosphate synthesis and degradation in human erythrocytes. (1974). https://pubmed.ncbi.nlm.nih.gov/4359937/ DOI: 10.1172/jci107607
    tissue_or_cell_type
    Plasma and erythrocytes
    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 631–642

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays · source_derived_draft · unverified_draft

    ### alcohol-low-plp-prevalence Thirty-five of 66 alcoholic subjects selected for normal liver function and haematology had plasma PLP below 5 ng/ml, the lowest value found in 94 controls. 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: More than half had less of the active vitamin than any healthy control, with healthy livers. organism: Human tissue_or_cell_type: Plasma and erythrocytes experimental_model: Plasma PLP in 66 alcoholic subjects without liver abnormality, plus erythrocyte enzyme assays limitations: Selecting subjects without abnormal liver function isolates the vitamin effect from liver disease. The phosphatase mechanism is shown in erythrocytes, not liver. exposure: Chronic alcohol abuse; acetaldehyde and ethanol applied to erythrocytes evidence_span: {"source_cache": "artifacts/alcohol-research/4359937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08", "start_char": 0, "end_char": 1650, "text_sha256": "1df4485150b1be55f3e5214c424f960ff627cfc317e643c86a0f6747efed8b08"} [alcohol-p4359937] Vitamin B6 metabolism in chronic alcohol abuse. Pyridoxal phosphate levels in plasma and the effects of acetaldehyde on pyridoxal phosphate synthesis and degradation in human erythrocytes. (1974). https://pubmed.ncbi.nlm.nih.gov/4359937/ DOI: 10.1172/jci107607
    Complete structured claim and evidence

  4. A defect of the mitochondrial respiratory chain was identified as a mechanism of reactive oxygen species overproduction in a rat model of alcoholic liver disease, with a role for zinc deficiency.

    Habitual alcohol consumption → Hepatic reactive oxygen species production source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/26585415.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c", "start_char": 0, "end_char": 1907, "text_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c"}
    experimental_model
    Rat model of alcoholic liver disease with mitochondrial respiratory chain assays
    exposure
    Chronic alcohol feeding with zinc status measured
    limitations
    Assigns the reactive oxygen species source to a respiratory chain defect and ties it to zinc. A rat model of the disease.
    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
    The damaged energy chain leaks reactive oxygen, and short zinc makes it worse.
    primary_references
    [alcohol-p26585415] Defect of mitochondrial respiratory chain is a mechanism of ROS overproduction in a rat model of alcoholic liver disease: role of zinc deficiency. (2016). https://pubmed.ncbi.nlm.nih.gov/26585415/ DOI: 10.1152/ajpgi.00270.2015
    tissue_or_cell_type
    Liver mitochondria

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 514–525

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat model of alcoholic liver disease with mitochondrial respiratory chain assays · source_derived_draft · unverified_draft

    ### alcohol-mitochondrial-ros A defect of the mitochondrial respiratory chain was identified as a mechanism of reactive oxygen species overproduction in a rat model of alcoholic liver disease, with a role for zinc deficiency. 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 damaged energy chain leaks reactive oxygen, and short zinc makes it worse. organism: Rat tissue_or_cell_type: Liver mitochondria experimental_model: Rat model of alcoholic liver disease with mitochondrial respiratory chain assays limitations: Assigns the reactive oxygen species source to a respiratory chain defect and ties it to zinc. A rat model of the disease. exposure: Chronic alcohol feeding with zinc status measured evidence_span: {"source_cache": "artifacts/alcohol-research/26585415.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c", "start_char": 0, "end_char": 1907, "text_sha256": "6743a8cefec8f9b3504ea8cc068c50c2b8fca42934fef4309d7e9819ff10d28c"} [alcohol-p26585415] Defect of mitochondrial respiratory chain is a mechanism of ROS overproduction in a rat model of alcoholic liver disease: role of zinc deficiency. (2016). https://pubmed.ncbi.nlm.nih.gov/26585415/ DOI: 10.1152/ajpgi.00270.2015
    Complete structured claim and evidence

  5. 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

  6. In vivo intestinal perfusion studies in alcoholic pigs showed reduced folate absorption.

    Habitual alcohol consumption → Intestinal folate uptake across the brush border source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/2596432.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "44f9e82990ef618c97924f29862366c0c718c3465edd42ceb1dc89e6bcda4e13", "start_char": 0, "end_char": 1018, "text_sha256": "44f9e82990ef618c97924f29862366c0c718c3465edd42ceb1dc89e6bcda4e13"}
    experimental_model
    In vivo intestinal perfusion in alcoholic pigs
    exposure
    Chronic alcohol feeding with in vivo perfusion
    limitations
    A whole-animal perfusion measurement rather than a membrane preparation, in a species with human-like intestinal physiology.
    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
    Pig
    plain_language
    Measured in a living gut, the absorption really is lower.
    primary_references
    [alcohol-p2596432] Folate absorption in alcoholic pigs: in vivo intestinal perfusion studies. (1989). https://pubmed.ncbi.nlm.nih.gov/2596432/ DOI: 10.1093/ajcn/50.6.1429
    tissue_or_cell_type
    Small intestine
    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 709–720

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vivo intestinal perfusion in alcoholic pigs · source_derived_draft · unverified_draft

    ### alcohol-pig-folate-absorption In vivo intestinal perfusion studies in alcoholic pigs showed reduced folate absorption. 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: Measured in a living gut, the absorption really is lower. organism: Pig tissue_or_cell_type: Small intestine experimental_model: In vivo intestinal perfusion in alcoholic pigs limitations: A whole-animal perfusion measurement rather than a membrane preparation, in a species with human-like intestinal physiology. exposure: Chronic alcohol feeding with in vivo perfusion evidence_span: {"source_cache": "artifacts/alcohol-research/2596432.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "44f9e82990ef618c97924f29862366c0c718c3465edd42ceb1dc89e6bcda4e13", "start_char": 0, "end_char": 1018, "text_sha256": "44f9e82990ef618c97924f29862366c0c718c3465edd42ceb1dc89e6bcda4e13"} [alcohol-p2596432] Folate absorption in alcoholic pigs: in vivo intestinal perfusion studies. (1989). https://pubmed.ncbi.nlm.nih.gov/2596432/ DOI: 10.1093/ajcn/50.6.1429
    Complete structured claim and evidence

  7. The ethanol-induced hepatic redox change was attenuated after chronic alcohol consumption in baboons, with metabolic consequences measured both in vivo and in vitro.

    Habitual alcohol consumption → Attenuation of the ethanol-induced hepatic redox change after chronic intake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/6793493.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe", "start_char": 0, "end_char": 986, "text_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe"}
    experimental_model
    Baboons fed alcohol chronically, with in vivo and in vitro redox measurement
    exposure
    Chronic alcohol consumption compared with acute administration
    limitations
    A primate chronic-feeding model. It shows the redox change is not fixed, which bears on reading any single acute measurement as the steady state.
    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
    Baboon
    plain_language
    The redox hit shrinks with habitual drinking, so a first-drink measurement does not describe a heavy drinker.
    primary_references
    [alcohol-p6793493] Attenuation of the ethanol-induced hepatic redox change after chronic alcohol consumption in baboons: metabolic consequences in vivo and in vitro. (1981). https://pubmed.ncbi.nlm.nih.gov/6793493/ DOI: 10.1002/hep.1840010106
    tissue_or_cell_type
    Liver

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 124–135

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Baboons fed alcohol chronically, with in vivo and in vitro redox measurement · source_derived_draft · unverified_draft

    ### alcohol-redox-adaptation The ethanol-induced hepatic redox change was attenuated after chronic alcohol consumption in baboons, with metabolic consequences measured both in vivo and in vitro. 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 redox hit shrinks with habitual drinking, so a first-drink measurement does not describe a heavy drinker. organism: Baboon tissue_or_cell_type: Liver experimental_model: Baboons fed alcohol chronically, with in vivo and in vitro redox measurement limitations: A primate chronic-feeding model. It shows the redox change is not fixed, which bears on reading any single acute measurement as the steady state. exposure: Chronic alcohol consumption compared with acute administration evidence_span: {"source_cache": "artifacts/alcohol-research/6793493.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe", "start_char": 0, "end_char": 986, "text_sha256": "5105956fd640dc7b32bd1d5e54a0df98bc5eb8d332220e27578ce5e631536fbe"} [alcohol-p6793493] Attenuation of the ethanol-induced hepatic redox change after chronic alcohol consumption in baboons: metabolic consequences in vivo and in vitro. (1981). https://pubmed.ncbi.nlm.nih.gov/6793493/ DOI: 10.1002/hep.1840010106
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The alcohol flush reaction is the result of excessive acetaldehyde accumulation, and the unpleasant symptoms tend to reduce alcohol consumption.

    Acetaldehyde → The alcohol flush reaction source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/2562960.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1", "start_char": 0, "end_char": 800, "text_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1"}
    experimental_model
    Polymerase chain reaction genotyping of 24 Japanese livers against enzyme phenotype
    exposure
    ALDH2 genotype compared with measured enzyme activity
    limitations
    Establishes dominance of the inactive allele, so heterozygotes are affected. The sample is 24 livers.
    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 flush is the body reacting to the first breakdown product, not to alcohol itself.
    primary_references
    [alcohol-p2562960] Genotypes for aldehyde dehydrogenase deficiency and alcohol sensitivity. The inactive ALDH2(2) allele is dominant. (1989). https://pubmed.ncbi.nlm.nih.gov/2562960/ DOI: 10.1172/jci113875
    tissue_or_cell_type
    Liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 163–174

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polymerase chain reaction genotyping of 24 Japanese livers against enzyme phenotype · source_derived_draft · unverified_draft

    ### alcohol-flush-from-acetaldehyde The alcohol flush reaction is the result of excessive acetaldehyde accumulation, and the unpleasant symptoms tend to reduce alcohol consumption. Condition category: machinery_impairment 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 flush is the body reacting to the first breakdown product, not to alcohol itself. organism: Human tissue_or_cell_type: Liver experimental_model: Polymerase chain reaction genotyping of 24 Japanese livers against enzyme phenotype limitations: Establishes dominance of the inactive allele, so heterozygotes are affected. The sample is 24 livers. exposure: ALDH2 genotype compared with measured enzyme activity evidence_span: {"source_cache": "artifacts/alcohol-research/2562960.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1", "start_char": 0, "end_char": 800, "text_sha256": "0f0722fad2747c7b723bce352582f07519b1b9b964edadb8674740458475efe1"} [alcohol-p2562960] Genotypes for aldehyde dehydrogenase deficiency and alcohol sensitivity. The inactive ALDH2(2) allele is dominant. (1989). https://pubmed.ncbi.nlm.nih.gov/2562960/ DOI: 10.1172/jci113875
    Complete structured claim and evidence

  2. Carriers of the ADH1B rs1229984 A-allele consumed 17.2% fewer units per week, had lower systolic blood pressure, interleukin-6, waist circumference and body mass index, and had lower odds of coronary heart disease (odds ratio 0.90), with the protective association the same across all categories of alcohol consumption.

    The ADH1B rs1229984 A-allele (ADH1B*2, Arg48His) → Coronary heart disease source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/25011450.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8f5f9f8c57fc5e32e827d8db1f212ebb427553d9b9f59db611a622bd99c4a10", "start_char": 0, "end_char": 1978, "text_sha256": "d8f5f9f8c57fc5e32e827d8db1f212ebb427553d9b9f59db611a622bd99c4a10"}
    experimental_model
    Mendelian randomisation meta-analysis of 56 studies and 261,991 individuals
    exposure
    The ADH1B rs1229984 variant as an instrument for alcohol exposure
    limitations
    Genetic instrument design, which avoids the confounding and reverse causation of consumption questionnaires. It cannot speak to drinking patterns the variant does not affect.
    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 gene variant that makes people drink less also gives them less heart disease, including among light drinkers.
    primary_references
    [alcohol-p25011450] Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. (2014). https://pubmed.ncbi.nlm.nih.gov/25011450/ DOI: 10.1136/bmj.g4164
    tissue_or_cell_type
    Cardiovascular system

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 566–577

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mendelian randomisation meta-analysis of 56 studies and 261,991 individuals · source_derived_draft · unverified_draft

    ### alcohol-mendelian-cardiovascular Carriers of the ADH1B rs1229984 A-allele consumed 17.2% fewer units per week, had lower systolic blood pressure, interleukin-6, waist circumference and body mass index, and had lower odds of coronary heart disease (odds ratio 0.90), with the protective association the same across all categories of alcohol consumption. 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 gene variant that makes people drink less also gives them less heart disease, including among light drinkers. organism: Human tissue_or_cell_type: Cardiovascular system experimental_model: Mendelian randomisation meta-analysis of 56 studies and 261,991 individuals limitations: Genetic instrument design, which avoids the confounding and reverse causation of consumption questionnaires. It cannot speak to drinking patterns the variant does not affect. exposure: The ADH1B rs1229984 variant as an instrument for alcohol exposure evidence_span: {"source_cache": "artifacts/alcohol-research/25011450.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d8f5f9f8c57fc5e32e827d8db1f212ebb427553d9b9f59db611a622bd99c4a10", "start_char": 0, "end_char": 1978, "text_sha256": "d8f5f9f8c57fc5e32e827d8db1f212ebb427553d9b9f59db611a622bd99c4a10"} [alcohol-p25011450] Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. (2014). https://pubmed.ncbi.nlm.nih.gov/25011450/ DOI: 10.1136/bmj.g4164
    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