Component
Eosinopenic response to ACTH
Eosinopenic response to ACTH. Experimental scope belongs to the associated record.
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
The 1958 depletion study found an impaired eosinopenic response to ACTH, while urinary 17-ketosteroid excretion remained normal; the authors did not interpret this pattern as sufficient evidence of adrenal cortical hypofunction.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Primary PDF pp.1643–1654; design, results and discussion.
- experimental_model
- Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls
- exposure
- Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.
- limitations
- Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. This historical indirect test is not a modern diagnostic assay for adrenal insufficiency.
- nutrient_topic
- Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
- organism
- Homo sapiens
- plain_language
- The altered hormone-response test did not establish adrenal failure.
- primary_references
- [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
- tissue_or_cell_type
- Whole-person symptoms, serum and urine
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1173–1185
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft
### b5-clin-acth-not-adrenal-diagnosis The 1958 depletion study found an impaired eosinopenic response to ACTH, while urinary 17-ketosteroid excretion remained normal; the authors did not interpret this pattern as sufficient evidence of adrenal cortical hypofunction. Condition category: nutrient_deficiency nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: The altered hormone-response test did not establish adrenal failure. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. This historical indirect test is not a modern diagnostic assay for adrenal insufficiency. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: false evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
Complete structured claim and evidenceAbnormal ACTH-associated eosinopenic responses in the two more heavily exposed men recovered after the antagonist was stopped and pantothenic acid was administered.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Primary PDF pp.1421–1425, especially Results and Summary.
- experimental_model
- Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet
- exposure
- One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal.
- limitations
- Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. Concurrent withdrawal prevents attributing recovery exclusively to vitamin administration.
- nutrient_topic
- Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
- organism
- Homo sapiens
- plain_language
- Recovery followed both removal of the antagonist and vitamin treatment.
- primary_references
- [b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918
- tissue_or_cell_type
- Whole-person clinical symptoms and functional tests
Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1215–1227
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet · source_derived_draft · unverified_draft
### b5-clin-antagonist-recovery Abnormal ACTH-associated eosinopenic responses in the two more heavily exposed men recovered after the antagonist was stopped and pantothenic acid was administered. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Recovery followed both removal of the antagonist and vitamin treatment. organism: Homo sapiens tissue_or_cell_type: Whole-person clinical symptoms and functional tests experimental_model: Historical four-man controlled antagonist experiment on a balanced 3200 kcal diet limitations: Pharmacological antagonist exposure with an otherwise normal diet, not dietary B5 deprivation. Very small sample and concurrent antagonist withdrawal prevent isolating a pure vitamin-rescue effect. Concurrent withdrawal prevents attributing recovery exclusively to vitamin administration. exposure: One control; three men received escalating antagonist regimens, up to 2–4 g/day in the highest-exposure subject; pantothenic acid 4 g/day was later given after antagonist withdrawal. cross_nutrient: false evidence_location: Primary PDF pp.1421–1425, especially Results and Summary. [b5-clin-hodges1959] Human pantothenic acid deficiency produced by omega-methyl pantothenic acid. (1959). https://pubmed.ncbi.nlm.nih.gov/13673099/ DOI: 10.1172/jci103918
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.