Component
Serum PTH concentration
Independent biological entity. Read linked claims for experimental scope and context.
10 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 it acts on
During early Mg repletion, PTH recovered before serum calcium normalized in the serially studied patients.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- Human hypomagnesemic hypocalcemia clinical study
- limitations
- Delay is indirect evidence for resistance and does not by itself identify a receptor or cyclase defect.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- Restoring the hormone signal did not immediately restore calcium; this pattern suggested an additional target-organ response problem.
- primary_references
- [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
- tissue_or_cell_type
- Blood; parathyroid-kidney axis
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 325–335
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human hypomagnesemic hypocalcemia clinical study · source_derived_draft · unverified_draft
### calcium-recovery-can-lag-pth-after-mg During early Mg repletion, PTH recovered before serum calcium normalized in the serially studied patients. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring the hormone signal did not immediately restore calcium; this pattern suggested an additional target-organ response problem. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid-kidney axis experimental_model: Human hypomagnesemic hypocalcemia clinical study limitations: Delay is indirect evidence for resistance and does not by itself identify a receptor or cyclase defect. cross_nutrient: magnesium -> PTH -> calcium [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
Complete structured claim and evidence
What acts on it
Mg administration promptly raised PTH in hypomagnesemic patients, whereas normal and hyperparathyroid comparison groups showed a decrease or little change.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- Acute Mg administration across clinical groups
- limitations
- Biphasic/status-dependent response does not establish one serum Mg breakpoint applicable to all patients.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- Restoring missing Mg can release a suppressed PTH response, while adding Mg in another starting state can inhibit it.
- primary_references
- [rude-1978-status-dependent-pth] Parathyroid hormone secretion in magnesium deficiency (1978). https://pubmed.ncbi.nlm.nih.gov/263326/ DOI: 10.1210/jcem-47-4-800
- tissue_or_cell_type
- Blood; parathyroid axis
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 349–359
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute Mg administration across clinical groups · source_derived_draft · unverified_draft
### mg-pth-response-depends-on-prior-status Mg administration promptly raised PTH in hypomagnesemic patients, whereas normal and hyperparathyroid comparison groups showed a decrease or little change. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring missing Mg can release a suppressed PTH response, while adding Mg in another starting state can inhibit it. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid axis experimental_model: Acute Mg administration across clinical groups limitations: Biphasic/status-dependent response does not establish one serum Mg breakpoint applicable to all patients. cross_nutrient: magnesium -> PTH -> calcium [rude-1978-status-dependent-pth] Parathyroid hormone secretion in magnesium deficiency (1978). https://pubmed.ncbi.nlm.nih.gov/263326/ DOI: 10.1210/jcem-47-4-800
Complete structured claim and evidenceAcute Mg administration increased circulating immunoreactive PTH within one minute in the three tested Mg-deficient patients.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- Human hypomagnesemic hypocalcemia clinical study
- limitations
- Three infusion experiments; timing supports but does not directly visualize secretory machinery.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- The fast hormone rise supports release of stored PTH after Mg restoration, rather than requiring new hormone synthesis first.
- primary_references
- [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
- tissue_or_cell_type
- Blood; parathyroid-kidney axis
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 313–323
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human hypomagnesemic hypocalcemia clinical study · source_derived_draft · unverified_draft
### mg-repletion-rapidly-releases-pth Acute Mg administration increased circulating immunoreactive PTH within one minute in the three tested Mg-deficient patients. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The fast hormone rise supports release of stored PTH after Mg restoration, rather than requiring new hormone synthesis first. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid-kidney axis experimental_model: Human hypomagnesemic hypocalcemia clinical study limitations: Three infusion experiments; timing supports but does not directly visualize secretory machinery. cross_nutrient: magnesium -> PTH -> calcium [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
Complete structured claim and evidenceAfter selective dietary Mg depletion, 20 of 26 adults showed unchanged or reduced PTH despite falling serum Mg and Ca.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- 26 initially normal adults before/after three-week low-Mg diet
- limitations
- Before/after experiment; not a population diagnostic rule. Depletion was supported by serum Mg, retention, and red-cell free Mg changes.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- PTH compensation was impaired during an induced shortage, before a failed calcium-replacement attempt was needed to reveal it.
- primary_references
- [fatemi-1991-selective-depletion] Effect of experimental human magnesium depletion on parathyroid hormone secretion and 1,25-dihydroxyvitamin D metabolism. (1991). https://pubmed.ncbi.nlm.nih.gov/1939521/ DOI: 10.1210/jcem-73-5-1067
- tissue_or_cell_type
- Blood; parathyroid and renal mineral axis
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 361–371
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 26 initially normal adults before/after three-week low-Mg diet · source_derived_draft · unverified_draft
### selective-mg-depletion-impairs-pth-compensation After selective dietary Mg depletion, 20 of 26 adults showed unchanged or reduced PTH despite falling serum Mg and Ca. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: PTH compensation was impaired during an induced shortage, before a failed calcium-replacement attempt was needed to reveal it. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid and renal mineral axis experimental_model: 26 initially normal adults before/after three-week low-Mg diet limitations: Before/after experiment; not a population diagnostic rule. Depletion was supported by serum Mg, retention, and red-cell free Mg changes. cross_nutrient: magnesium -> PTH -> calcium [fatemi-1991-selective-depletion] Effect of experimental human magnesium depletion on parathyroid hormone secretion and 1,25-dihydroxyvitamin D metabolism. (1991). https://pubmed.ncbi.nlm.nih.gov/1939521/ DOI: 10.1210/jcem-73-5-1067
Complete structured claim and evidenceMost untreated patients in the clinical series had normal or undetectable immunoreactive PTH despite severe hypocalcemia.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium
- experimental_model
- Human hypomagnesemic hypocalcemia clinical study
- limitations
- Observational baseline result; older immunoreactive PTH assays differ from modern intact-PTH methods.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- A PTH value within a laboratory reference range can still be too low for someone whose calcium is very low.
- primary_references
- [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
- tissue_or_cell_type
- Blood; parathyroid-kidney axis
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 301–311
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human hypomagnesemic hypocalcemia clinical study · source_derived_draft · unverified_draft
### severe-mg-deficiency-inadequate-pth-response Most untreated patients in the clinical series had normal or undetectable immunoreactive PTH despite severe hypocalcemia. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A PTH value within a laboratory reference range can still be too low for someone whose calcium is very low. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid-kidney axis experimental_model: Human hypomagnesemic hypocalcemia clinical study limitations: Observational baseline result; older immunoreactive PTH assays differ from modern intact-PTH methods. cross_nutrient: magnesium -> PTH -> calcium [rude-1976-human-pth-resistance] Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency (1976). https://pubmed.ncbi.nlm.nih.gov/182417/ DOI: 10.1111/j.1365-2265.1976.tb01947.x
Complete structured claim and evidencePTH suppression did not differ significantly among the three vitamin D regimens given with calcium.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- cross_nutrient
- true
- experimental_model
- Six-week randomized comparison in 40 infants/toddlers with 25(OH)D<20 ng/mL; all prescribed calcium
- exposure
- D2 2000 IU/day, D2 50, 000 IU/week or D3 2000 IU/day for 6 weeks; all also 50 mg/kg/day elemental calcium.
- limitations
- Small pediatric trial; D and calcium effects cannot be separated; biochemical outcomes do not establish long-term comparative safety.
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Homo sapiens
- plain_language
- The hormone response was not detectably different between these treatment groups.
- primary_references
- [gordon2008] Treatment of hypovitaminosis D in infants and toddlers. (2008). https://pubmed.ncbi.nlm.nih.gov/18413426/ DOI: 10.1210/jc.2007-2790
- tissue_or_cell_type
- Human circulating measurements
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1483–1494
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-week randomized comparison in 40 infants/toddlers with 25(OH)D<20 ng/mL; all prescribed calcium · source_derived_draft · unverified_draft
### vd-gordon-pth PTH suppression did not differ significantly among the three vitamin D regimens given with calcium. Condition category: biomarker_context nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The hormone response was not detectably different between these treatment groups. organism: Homo sapiens tissue_or_cell_type: Human circulating measurements experimental_model: Six-week randomized comparison in 40 infants/toddlers with 25(OH)D<20 ng/mL; all prescribed calcium limitations: Small pediatric trial; D and calcium effects cannot be separated; biochemical outcomes do not establish long-term comparative safety. exposure: D2 2000 IU/day, D2 50, 000 IU/week or D3 2000 IU/day for 6 weeks; all also 50 mg/kg/day elemental calcium. cross_nutrient: true [gordon2008] Treatment of hypovitaminosis D in infants and toddlers. (2008). https://pubmed.ncbi.nlm.nih.gov/18413426/ DOI: 10.1210/jc.2007-2790
Complete structured claim and evidenceReducing calcium intake from 2000 to 300 mg/day increased intact PTH within one week in nine healthy women.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Nine healthy women; controlled 2000-to-300 mg/day calcium diet change and oral 47Ca retention
- limitations
- Small controlled study; low intake is not proof of symptomatic deficiency.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- Low intake recruits a hormonal response.
- primary_references
- [dawsonhughes1988] Effect of lowering dietary calcium intake on fractional whole body calcium retention (1988). https://pubmed.ncbi.nlm.nih.gov/3132484/ DOI: 10.1210/jcem-67-1-62
- tissue_or_cell_type
- Blood
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 291–300
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nine healthy women; controlled 2000-to-300 mg/day calcium diet change and oral 47Ca retention · source_derived_draft · unverified_draft
### low-calcium-intake-increases-pth Reducing calcium intake from 2000 to 300 mg/day increased intact PTH within one week in nine healthy women. Condition category: nutrient_deficiency nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low intake recruits a hormonal response. organism: Homo sapiens tissue_or_cell_type: Blood experimental_model: Nine healthy women; controlled 2000-to-300 mg/day calcium diet change and oral 47Ca retention limitations: Small controlled study; low intake is not proof of symptomatic deficiency. [dawsonhughes1988] Effect of lowering dietary calcium intake on fractional whole body calcium retention (1988). https://pubmed.ncbi.nlm.nih.gov/3132484/ DOI: 10.1210/jcem-67-1-62
Complete structured claim and evidenceThe tested boron and magnesium dietary treatments did not significantly affect serum PTH in the 2004 study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/boron-research/15724868.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7009311021e781ba9b1e9a9244c081cf20700511cc8704e8294b1a2c55dc0e24", "start_char": 0, "end_char": 2138, "text_sha256": "7009311021e781ba9b1e9a9244c081cf20700511cc8704e8294b1a2c55dc0e24"}
- experimental_model
- Double-blind Latin-square metabolic-unit feeding in 13 postmenopausal women
- exposure
- Approximately 118 versus 318 mg Mg/day and 0.25 versus 3.25 mg B/day; 42-day periods
- limitations
- Boron had no obvious overall effect on the response to magnesium deprivation. Results cannot establish boron as a treatment for hypomagnesemia or a substitute for magnesium.
- nutrient_topic
- Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
- organism
- Human
- plain_language
- The study did not demonstrate that boron improves mineral balance by raising or lowering PTH.
- primary_references
- [boron-p15724868] The alteration of magnesium, calcium and phosphorus metabolism by dietary magnesium deprivation in postmenopausal women is not affected by dietary boron deprivation. (2004). https://pubmed.ncbi.nlm.nih.gov/15724868/
- tissue_or_cell_type
- Mineral balance and endocrine measurements
Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 781–792
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind Latin-square metabolic-unit feeding in 13 postmenopausal women · source_derived_draft · unverified_draft
### boron-pth-null-2004 The tested boron and magnesium dietary treatments did not significantly affect serum PTH in the 2004 study. Condition category: normal nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The study did not demonstrate that boron improves mineral balance by raising or lowering PTH. organism: Human tissue_or_cell_type: Mineral balance and endocrine measurements experimental_model: Double-blind Latin-square metabolic-unit feeding in 13 postmenopausal women limitations: Boron had no obvious overall effect on the response to magnesium deprivation. Results cannot establish boron as a treatment for hypomagnesemia or a substitute for magnesium. exposure: Approximately 118 versus 318 mg Mg/day and 0.25 versus 3.25 mg B/day; 42-day periods evidence_span: {"source_cache": "artifacts/boron-research/15724868.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7009311021e781ba9b1e9a9244c081cf20700511cc8704e8294b1a2c55dc0e24", "start_char": 0, "end_char": 2138, "text_sha256": "7009311021e781ba9b1e9a9244c081cf20700511cc8704e8294b1a2c55dc0e24"} [boron-p15724868] The alteration of magnesium, calcium and phosphorus metabolism by dietary magnesium deprivation in postmenopausal women is not affected by dietary boron deprivation. (2004). https://pubmed.ncbi.nlm.nih.gov/15724868/
Complete structured claim and evidencePTH increased in the ferric-carboxymaltose-associated phosphate-wasting cascade.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/30518682.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d", "start_char": 0, "end_char": 2381, "text_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d"}
- experimental_model
- Randomized iron-formulation comparison with physiological substudy
- exposure
- One trial course of ferric carboxymaltose or ferumoxytol; follow-up five weeks
- limitations
- Formulation-specific drug effect, not dietary iron. FGF23 was associated with the downstream changes; the exact reason the formulations differ was not settled.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Human
- plain_language
- The parathyroid response added another hormone affecting renal phosphate handling.
- primary_references
- [phosphorus-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
- tissue_or_cell_type
- Iron-deficiency anemia; n=1997 parent trial, n=185 substudy
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 1037–1048
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized iron-formulation comparison with physiological substudy · source_derived_draft · unverified_draft
### phosphorus-iron-pth PTH increased in the ferric-carboxymaltose-associated phosphate-wasting cascade. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The parathyroid response added another hormone affecting renal phosphate handling. organism: Human tissue_or_cell_type: Iron-deficiency anemia; n=1997 parent trial, n=185 substudy experimental_model: Randomized iron-formulation comparison with physiological substudy limitations: Formulation-specific drug effect, not dietary iron. FGF23 was associated with the downstream changes; the exact reason the formulations differ was not settled. exposure: One trial course of ferric carboxymaltose or ferumoxytol; follow-up five weeks evidence_span: {"source_cache": "artifacts/phosphorus-research/30518682.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d", "start_char": 0, "end_char": 2381, "text_sha256": "e1d37261355eedeff60d9715e7eb88b6718641ed868c5b3ab64fceaf62c15e6d"} [phosphorus-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
Complete structured claim and evidencePTH declined during the higher-phosphate/calcium regimen even while FGF23 increased.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/21030580.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e", "start_char": 0, "end_char": 1603, "text_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e"}
- experimental_model
- Paired 36-hour dietary interventions
- exposure
- Low/high phosphate and calcium diets, separated by a week
- limitations
- Both calcium and phosphate changed; phosphate alone cannot be assigned the full effect. Timing and circadian variation matter.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Human
- plain_language
- Changing calcium alongside phosphate produced a different PTH pattern than a phosphate-only cell challenge.
- primary_references
- [phosphorus-p21030580] Effects of dietary phosphate and calcium intake on fibroblast growth factor-23. (2011). https://pubmed.ncbi.nlm.nih.gov/21030580/ DOI: 10.2215/cjn.04730510
- tissue_or_cell_type
- Ten healthy adults; serial serum measurements and 24-hour urine
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 972–983
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Paired 36-hour dietary interventions · source_derived_draft · unverified_draft
### phosphorus-mixed-diet-pth PTH declined during the higher-phosphate/calcium regimen even while FGF23 increased. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing calcium alongside phosphate produced a different PTH pattern than a phosphate-only cell challenge. organism: Human tissue_or_cell_type: Ten healthy adults; serial serum measurements and 24-hour urine experimental_model: Paired 36-hour dietary interventions limitations: Both calcium and phosphate changed; phosphate alone cannot be assigned the full effect. Timing and circadian variation matter. exposure: Low/high phosphate and calcium diets, separated by a week evidence_span: {"source_cache": "artifacts/phosphorus-research/21030580.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e", "start_char": 0, "end_char": 1603, "text_sha256": "e51a1cd580ac4ea7b0232f65c73ac0814df6bff655bf7bd6d0d82f7f9f21a33e"} [phosphorus-p21030580] Effects of dietary phosphate and calcium intake on fibroblast growth factor-23. (2011). https://pubmed.ncbi.nlm.nih.gov/21030580/ DOI: 10.2215/cjn.04730510
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.