Component
Blood acetaldehyde concentration
Blood acetaldehyde concentration. Species, exposure and limitations are retained in each linked claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
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.
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
Where it participates (unsigned role)
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.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.