Component

The ADH1B rs1229984 A-allele (ADH1B*2, Arg48His)

The ADH1B rs1229984 A-allele (ADH1B*2, Arg48His). 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. An animal model developed to test the mechanism of protection against alcoholism by an alcohol dehydrogenase polymorphism supports faster ethanol oxidation producing higher acetaldehyde as the protective step.

    The ADH1B rs1229984 A-allele (ADH1B*2, Arg48His) → Blood acetaldehyde concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/19710201.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22b9547745b08adaa8a9a722228e9c5987ac67442b20f2737d8c54f6988ec7c5", "start_char": 0, "end_char": 1426, "text_sha256": "22b9547745b08adaa8a9a722228e9c5987ac67442b20f2737d8c54f6988ec7c5"}
    experimental_model
    An animal model built to reproduce the human alcohol dehydrogenase polymorphism
    exposure
    Higher-activity alcohol dehydrogenase against voluntary intake
    limitations
    A constructed animal model of a human protective genotype. It supports the acetaldehyde-burst explanation; it is not a human trial.
    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 model of the human variant
    plain_language
    A faster first enzyme makes the unpleasant metabolite arrive sooner.
    primary_references
    [alcohol-p19710201] Mechanism of protection against alcoholism by an alcohol dehydrogenase polymorphism: development of an animal model. (2010). https://pubmed.ncbi.nlm.nih.gov/19710201/ DOI: 10.1096/fj.09-132563
    tissue_or_cell_type
    Liver and behaviour
    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 189–200

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · An animal model built to reproduce the human alcohol dehydrogenase polymorphism · source_derived_draft · unverified_draft

    ### alcohol-adh1b-fast-oxidation An animal model developed to test the mechanism of protection against alcoholism by an alcohol dehydrogenase polymorphism supports faster ethanol oxidation producing higher acetaldehyde as the protective step. 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: A faster first enzyme makes the unpleasant metabolite arrive sooner. organism: Rat model of the human variant tissue_or_cell_type: Liver and behaviour experimental_model: An animal model built to reproduce the human alcohol dehydrogenase polymorphism limitations: A constructed animal model of a human protective genotype. It supports the acetaldehyde-burst explanation; it is not a human trial. exposure: Higher-activity alcohol dehydrogenase against voluntary intake evidence_span: {"source_cache": "artifacts/alcohol-research/19710201.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "22b9547745b08adaa8a9a722228e9c5987ac67442b20f2737d8c54f6988ec7c5", "start_char": 0, "end_char": 1426, "text_sha256": "22b9547745b08adaa8a9a722228e9c5987ac67442b20f2737d8c54f6988ec7c5"} [alcohol-p19710201] Mechanism of protection against alcoholism by an alcohol dehydrogenase polymorphism: development of an animal model. (2010). https://pubmed.ncbi.nlm.nih.gov/19710201/ DOI: 10.1096/fj.09-132563
    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

Where it participates (unsigned role)

  1. ALDH2*2 but not ADH1B*2 is the causative variant allele for Asian alcohol flushing after a low-dose challenge, on correlated pharmacokinetic and pharmacodynamic findings.

    The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487 → 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/25365528.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218", "start_char": 0, "end_char": 1803, "text_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218"}
    experimental_model
    Low-dose alcohol challenge in genotyped subjects with paired pharmacokinetics and pharmacodynamics
    exposure
    Low-dose alcohol challenge across ADH1B and ALDH2 genotypes
    limitations
    Separates the two candidate variants by measuring both blood levels and symptoms. A low-dose challenge may not represent ordinary drinking.
    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
    Of the two variants people blame for flushing, only one actually causes it.
    primary_references
    [alcohol-p25365528] ALDH2*2 but not ADH1B*2 is a causative variant gene allele for Asian alcohol flushing after a low-dose challenge: correlation of the pharmacokinetic and pharmacodynamic findings. (2014). https://pubmed.ncbi.nlm.nih.gov/25365528/ DOI: 10.1097/fpc.0000000000000096
    tissue_or_cell_type
    Whole body
    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 176–187

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Low-dose alcohol challenge in genotyped subjects with paired pharmacokinetics and pharmacodynamics · source_derived_draft · unverified_draft

    ### alcohol-aldh2-not-adh1b-flush ALDH2*2 but not ADH1B*2 is the causative variant allele for Asian alcohol flushing after a low-dose challenge, on correlated pharmacokinetic and pharmacodynamic findings. 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: Of the two variants people blame for flushing, only one actually causes it. organism: Human tissue_or_cell_type: Whole body experimental_model: Low-dose alcohol challenge in genotyped subjects with paired pharmacokinetics and pharmacodynamics limitations: Separates the two candidate variants by measuring both blood levels and symptoms. A low-dose challenge may not represent ordinary drinking. exposure: Low-dose alcohol challenge across ADH1B and ALDH2 genotypes evidence_span: {"source_cache": "artifacts/alcohol-research/25365528.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218", "start_char": 0, "end_char": 1803, "text_sha256": "74fa331e891fe46dedf3789025686318b37eae41389f093bda084e4a6d482218"} [alcohol-p25365528] ALDH2*2 but not ADH1B*2 is a causative variant gene allele for Asian alcohol flushing after a low-dose challenge: correlation of the pharmacokinetic and pharmacodynamic findings. (2014). https://pubmed.ncbi.nlm.nih.gov/25365528/ DOI: 10.1097/fpc.0000000000000096
    Complete structured claim and evidence

  2. Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhanced oesophageal cancer risk.

    The inactive ALDH2*2 subunit carrying lysine for glutamate at position 487 → Oesophageal squamous cell cancer risk source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/19698717.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58", "start_char": 0, "end_char": 1706, "text_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58"}
    experimental_model
    Case-control study of oesophageal cancer with ADH1B and ALDH2 genotypes and smoking
    exposure
    Alcohol consumption and smoking across functional genotypes
    limitations
    A gene-environment interaction study. Synergy is reported on a statistical interaction scale, and the design is case-control.
    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 variant that makes drinking unpleasant also makes each drink more carcinogenic.
    primary_references
    [alcohol-p19698717] Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk. (2009). https://pubmed.ncbi.nlm.nih.gov/19698717/ DOI: 10.1053/j.gastro.2009.07.070
    tissue_or_cell_type
    Oesophagus
    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 540–551

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case-control study of oesophageal cancer with ADH1B and ALDH2 genotypes and smoking · source_derived_draft · unverified_draft

    ### alcohol-genotype-cancer-synergy Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhanced oesophageal cancer risk. 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 variant that makes drinking unpleasant also makes each drink more carcinogenic. organism: Human tissue_or_cell_type: Oesophagus experimental_model: Case-control study of oesophageal cancer with ADH1B and ALDH2 genotypes and smoking limitations: A gene-environment interaction study. Synergy is reported on a statistical interaction scale, and the design is case-control. exposure: Alcohol consumption and smoking across functional genotypes evidence_span: {"source_cache": "artifacts/alcohol-research/19698717.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58", "start_char": 0, "end_char": 1706, "text_sha256": "4262a0549d8e78b4e7719f62bfa61849f3cf6eb3403bf45fe28d32b7d7662c58"} [alcohol-p19698717] Functional variants in ADH1B and ALDH2 coupled with alcohol and smoking synergistically enhance esophageal cancer risk. (2009). https://pubmed.ncbi.nlm.nih.gov/19698717/ DOI: 10.1053/j.gastro.2009.07.070
    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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