Component
Visual sensitivity
Visual sensitivity; measured endpoint and experimental scope are stated in linked claims.
3 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
Visual function normalized within eight days of vitamin A treatment in the three reported deficient patients.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Before/after repletion follow-up
- limitations
- Uncontrolled treatment observation; no dose recommendation.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens
- plain_language
- Repletion reversed the measured visual deficit in this series.
- primary_references
- [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
- tissue_or_cell_type
- Retina
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1019–1028
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Before/after repletion follow-up · source_derived_draft · unverified_draft
### a-vision-deficiency-repletion Visual function normalized within eight days of vitamin A treatment in the three reported deficient patients. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Repletion reversed the measured visual deficit in this series. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Before/after repletion follow-up limitations: Uncontrolled treatment observation; no dose recommendation. [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
Complete structured claim and evidenceAll three deficient patients initially lacked measurable rod function and had delayed cone adaptation.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Baseline visual function
- limitations
- Clinical series of three, not a population effect size.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens
- plain_language
- Severe depletion impaired night vision and also slowed cone recovery.
- primary_references
- [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
- tissue_or_cell_type
- Retina
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1008–1017
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Baseline visual function · source_derived_draft · unverified_draft
### a-vision-deficiency-sensitivity All three deficient patients initially lacked measurable rod function and had delayed cone adaptation. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe depletion impaired night vision and also slowed cone recovery. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Baseline visual function limitations: Clinical series of three, not a population effect size. [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
Complete structured claim and evidenceLrat-null mice had severely attenuated rod and cone visual function by electroretinography and pupil-response testing.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Electroretinography and pupillary constriction
- limitations
- The phenotype tests a genetic esterification defect.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus
- plain_language
- Loss of retinol esterification impaired measured vision.
- primary_references
- [batten-2004] Lecithin-retinol acyltransferase is essential for accumulation of all-trans-retinyl esters in the eye and in the liver (2004). https://pubmed.ncbi.nlm.nih.gov/14684738/ DOI: 10.1074/jbc.M312410200
- tissue_or_cell_type
- Eye
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 712–721
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electroretinography and pupillary constriction · source_derived_draft · unverified_draft
### a-vision-lrat-visual-function Lrat-null mice had severely attenuated rod and cone visual function by electroretinography and pupil-response testing. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of retinol esterification impaired measured vision. organism: Mus musculus tissue_or_cell_type: Eye experimental_model: Electroretinography and pupillary constriction limitations: The phenotype tests a genetic esterification defect. [batten-2004] Lecithin-retinol acyltransferase is essential for accumulation of all-trans-retinyl esters in the eye and in the liver (2004). https://pubmed.ncbi.nlm.nih.gov/14684738/ DOI: 10.1074/jbc.M312410200
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.