Component
Erythroid cell production
Measured process or biological entity; consult each linked claim for the experimental scope.
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
All six patients developed anemia; the study described low reticulocytes and erythroid suppression with recovery during riboflavin replacement.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Iron supply alone did not prevent anemia in the combined B2 restriction/antagonist experiment.
- experimental_model
- Historical induced-depletion study in six men with inoperable cancers; no healthy randomized control group.
- exposure
- Low-riboflavin semisynthetic diet plus galactoflavin antagonist, followed by riboflavin replacement; three also received oral antibiotics.
- limitations
- Same six-patient experiment as lesion record; other nutrients were supplied but cancer and antagonist effects limit causal generalization.
- nutrient_topic
- Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
- organism
- Homo sapiens
- plain_language
- Severe induced shortage reduced new red-cell production; the anemia was not simply assumed to be low dietary iron.
- primary_references
- [b2-lane1964] THE RAPID INDUCTION OF HUMAN RIBOFLAVIN DEFICIENCY WITH GALACTOFLAVIN (1964). https://pubmed.ncbi.nlm.nih.gov/14135487/ DOI: 10.1172/jci104921
- tissue_or_cell_type
- Bone marrow and circulating erythrocytes
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1801–1812
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical induced-depletion study in six men with inoperable cancers; no healthy randomized control group. · source_derived_draft · unverified_draft
### b2-induced-erythroid-suppression All six patients developed anemia; the study described low reticulocytes and erythroid suppression with recovery during riboflavin replacement. Condition category: nutrient_deficiency nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe induced shortage reduced new red-cell production; the anemia was not simply assumed to be low dietary iron. organism: Homo sapiens tissue_or_cell_type: Bone marrow and circulating erythrocytes experimental_model: Historical induced-depletion study in six men with inoperable cancers; no healthy randomized control group. limitations: Same six-patient experiment as lesion record; other nutrients were supplied but cancer and antagonist effects limit causal generalization. exposure: Low-riboflavin semisynthetic diet plus galactoflavin antagonist, followed by riboflavin replacement; three also received oral antibiotics. cross_nutrient: Iron supply alone did not prevent anemia in the combined B2 restriction/antagonist experiment. [b2-lane1964] THE RAPID INDUCTION OF HUMAN RIBOFLAVIN DEFICIENCY WITH GALACTOFLAVIN (1964). https://pubmed.ncbi.nlm.nih.gov/14135487/ DOI: 10.1172/jci104921
Complete structured claim and evidenceIn two patients with induced B2 deficiency, parenteral iron did not trigger reticulocytosis, whereas subsequent riboflavin did.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Documented failure of iron response in a specific induced B2-deficiency setting.
- experimental_model
- Historical induced-depletion study in six men with inoperable cancers; no healthy randomized control group.
- exposure
- Low-riboflavin semisynthetic diet plus galactoflavin antagonist, followed by riboflavin replacement; three also received oral antibiotics.
- limitations
- Two cases within a six-person cancer/galactoflavin experiment; cannot generalize this to every anemia or infer a modern treatment regimen.
- nutrient_topic
- Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
- organism
- Homo sapiens
- plain_language
- More iron did not restore new red-cell production while usable B2 was severely limited in these cases.
- primary_references
- [b2-lane1964] THE RAPID INDUCTION OF HUMAN RIBOFLAVIN DEFICIENCY WITH GALACTOFLAVIN (1964). https://pubmed.ncbi.nlm.nih.gov/14135487/ DOI: 10.1172/jci104921
- tissue_or_cell_type
- Circulating reticulocytes
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1814–1825
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical induced-depletion study in six men with inoperable cancers; no healthy randomized control group. · source_derived_draft · unverified_draft
### b2-induced-iron-response-failure In two patients with induced B2 deficiency, parenteral iron did not trigger reticulocytosis, whereas subsequent riboflavin did. Condition category: nutrient_deficiency nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: More iron did not restore new red-cell production while usable B2 was severely limited in these cases. organism: Homo sapiens tissue_or_cell_type: Circulating reticulocytes experimental_model: Historical induced-depletion study in six men with inoperable cancers; no healthy randomized control group. limitations: Two cases within a six-person cancer/galactoflavin experiment; cannot generalize this to every anemia or infer a modern treatment regimen. exposure: Low-riboflavin semisynthetic diet plus galactoflavin antagonist, followed by riboflavin replacement; three also received oral antibiotics. cross_nutrient: Documented failure of iron response in a specific induced B2-deficiency setting. [b2-lane1964] THE RAPID INDUCTION OF HUMAN RIBOFLAVIN DEFICIENCY WITH GALACTOFLAVIN (1964). https://pubmed.ncbi.nlm.nih.gov/14135487/ DOI: 10.1172/jci104921
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.