Component
Serum calcium concentration
Independent biological entity. Read linked claims for experimental scope and context.
14 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
Mice with intestinal Vdr deletion maintained serum calcium despite calcium malabsorption and impaired skeletal mineral storage.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- experimental_model
- Intestinal and osteoblast Vdr deletion, low-calcium diets, and skeletal assays in growing mice
- limitations
- Growing-mouse genetic model; not a validated human dietary diagnostic.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Mus musculus
- plain_language
- Normal blood calcium can coexist with inadequate skeletal supply.
- primary_references
- [lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3336970/ DOI: 10.1172/JCI45890
- research_relationship_category
- biomarker
- tissue_or_cell_type
- Blood, intestine and skeleton
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 337–347
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal and osteoblast Vdr deletion, low-calcium diets, and skeletal assays in growing mice · source_derived_draft · unverified_draft
### normal-serum-calcium-does-not-establish-sufficiency Mice with intestinal Vdr deletion maintained serum calcium despite calcium malabsorption and impaired skeletal mineral storage. Condition category: biomarker_context nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Normal blood calcium can coexist with inadequate skeletal supply. organism: Mus musculus tissue_or_cell_type: Blood, intestine and skeleton experimental_model: Intestinal and osteoblast Vdr deletion, low-calcium diets, and skeletal assays in growing mice limitations: Growing-mouse genetic model; not a validated human dietary diagnostic. research_relationship_category: biomarker [lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3336970/ DOI: 10.1172/JCI45890
Complete structured claim and evidence
What acts on it
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 evidenceIntestinal Trpm7 deletion reduced serum and bone calcium in suckling mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- TRPM7 is shared machinery for magnesium and calcium handling in this developmental model; causal Mg-to-Ca nutritional dependence was not isolated.
- evidence-system
- Conditional knockout; postnatal mineral phenotyping
- experimental_model
- Conditional knockout; postnatal mineral phenotyping
- limitations
- Shared channel loss; does not prove low Mg intake causes calcium malabsorption.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Mouse
- plain_language
- The same epithelial channel machinery supports calcium as well as magnesium supply.
- primary_references
- [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
- tissue
- Intestine; serum and bone
- tissue_or_cell_type
- Intestine; serum and bone
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 988–1000
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional knockout; postnatal mineral phenotyping · source_derived_draft · unverified_draft
### intestinal-trpm7-loss-calcium Intestinal Trpm7 deletion reduced serum and bone calcium in suckling mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same epithelial channel machinery supports calcium as well as magnesium supply. organism: Mouse tissue_or_cell_type: Intestine; serum and bone experimental_model: Conditional knockout; postnatal mineral phenotyping limitations: Shared channel loss; does not prove low Mg intake causes calcium malabsorption. cross_nutrient: TRPM7 is shared machinery for magnesium and calcium handling in this developmental model; causal Mg-to-Ca nutritional dependence was not isolated. evidence-system: Conditional knockout; postnatal mineral phenotyping tissue: Intestine; serum and bone [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
Complete structured claim and evidenceMagnesium treatment normalized mean serum calcium, while calcitriol rose into or above normal in only five of the 23 patients.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Magnesium -> calcium response; vitamin D normalization is not obligatory in this cohort.
- experimental_model
- Five to thirteen days of parenteral Mg.
- limitations
- Nonrandomized clinical response; calcium recovery does not prove that calcitriol rose.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- Restoring magnesium did not automatically normalize every vitamin D result.
- primary_references
- [mg-rude1985] Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency (1985). https://pubmed.ncbi.nlm.nih.gov/3840173/ DOI: 10.1210/jcem-61-5-933
- tissue_or_cell_type
- Human serum; circulating mineral and vitamin D metabolites
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1358–1368
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five to thirteen days of parenteral Mg. · source_derived_draft · unverified_draft
### mg-calcium-recovery-precedes-calcitriol Magnesium treatment normalized mean serum calcium, while calcitriol rose into or above normal in only five of the 23 patients. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring magnesium did not automatically normalize every vitamin D result. organism: Homo sapiens tissue_or_cell_type: Human serum; circulating mineral and vitamin D metabolites experimental_model: Five to thirteen days of parenteral Mg. limitations: Nonrandomized clinical response; calcium recovery does not prove that calcitriol rose. cross_nutrient: Magnesium -> calcium response; vitamin D normalization is not obligatory in this cohort. [mg-rude1985] Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency (1985). https://pubmed.ncbi.nlm.nih.gov/3840173/ DOI: 10.1210/jcem-61-5-933
Complete structured claim and evidenceA child with primary hypomagnesemia retained calcemic and renal phosphate/cAMP responses to parathyroid extract during Mg depletion despite impaired endogenous PTH secretion.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> PTH -> calcium/phosphate
- experimental_model
- Single-child Mg withdrawal/repletion with hormone challenge
- limitations
- Single case; shows PTH resistance is not obligatory. Primary hypomagnesemia was not genetically assigned in this study.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- In this child the main failure was releasing the hormone; tissues could still respond when hormone was provided.
- primary_references
- [suh-1973-preserved-pth-response] Pathogenesis of Hypocalcemia in Primary Hypomagnesemia: Normal End-Organ Responsiveness to Parathyroid Hormone, Impaired Parathyroid Gland Function (1973). https://www.jci.org/articles/view/107159 DOI: 10.1172/JCI107159
- tissue_or_cell_type
- Blood and kidney
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 397–407
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single-child Mg withdrawal/repletion with hormone challenge · source_derived_draft · unverified_draft
### primary-hypomagnesemia-can-preserve-pth-response A child with primary hypomagnesemia retained calcemic and renal phosphate/cAMP responses to parathyroid extract during Mg depletion despite impaired endogenous PTH secretion. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this child the main failure was releasing the hormone; tissues could still respond when hormone was provided. organism: Homo sapiens tissue_or_cell_type: Blood and kidney experimental_model: Single-child Mg withdrawal/repletion with hormone challenge limitations: Single case; shows PTH resistance is not obligatory. Primary hypomagnesemia was not genetically assigned in this study. cross_nutrient: magnesium -> PTH -> calcium/phosphate [suh-1973-preserved-pth-response] Pathogenesis of Hypocalcemia in Primary Hypomagnesemia: Normal End-Organ Responsiveness to Parathyroid Hormone, Impaired Parathyroid Gland Function (1973). https://www.jci.org/articles/view/107159 DOI: 10.1172/JCI107159
Complete structured claim and evidenceThree weeks of selective Mg depletion produced a small but significant reduction in serum calcium in the adult study.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- magnesium -> calcium
- experimental_model
- 26 initially normal adults before/after three-week low-Mg diet
- limitations
- Mean change in a small controlled study; not evidence that every mildly low Mg value causes clinical hypocalcemia.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Homo sapiens
- plain_language
- Calcium regulation changed during experimental Mg shortage even without a preceding calcium-repletion failure.
- 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 373–383
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-lowers-circulating-calcium Three weeks of selective Mg depletion produced a small but significant reduction in serum calcium in the adult study. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium regulation changed during experimental Mg shortage even without a preceding calcium-repletion failure. 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: Mean change in a small controlled study; not evidence that every mildly low Mg value causes clinical hypocalcemia. cross_nutrient: magnesium -> 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 evidenceRecessive CYP24A1 variants were identified in infants with hypercalcemia, including a second group whose illness followed high-dose vitamin D prophylaxis.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion.
- experimental_model
- Human candidate-gene study with supporting enzyme assays
- exposure
- First cohort received 500 IU/day; second cohort became symptomatic 2-3 weeks after intermittent high-dose prophylaxis.
- limitations
- Selected families do not estimate population risk. Genotype, dose and penetrance matter; this is not a universal safe/unsafe serum or dose threshold.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- 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
- Defective vitamin D breakdown can make infants unusually sensitive to supplementation.
- primary_references
- [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
- tissue_or_cell_type
- systemic calcium handling
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 602–615
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human candidate-gene study with supporting enzyme assays · source_derived_draft · unverified_draft
### vd-act-cyp24a1-hypercalcemia Recessive CYP24A1 variants were identified in infants with hypercalcemia, including a second group whose illness followed high-dose vitamin D prophylaxis. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Defective vitamin D breakdown can make infants unusually sensitive to supplementation. organism: Homo sapiens tissue_or_cell_type: systemic calcium handling experimental_model: Human candidate-gene study with supporting enzyme assays limitations: Selected families do not estimate population risk. Genotype, dose and penetrance matter; this is not a universal safe/unsafe serum or dose threshold. exposure: First cohort received 500 IU/day; second cohort became symptomatic 2-3 weeks after intermittent high-dose prophylaxis. cross_nutrient: true evidence_location: Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion. nutrient: Vitamin D2 and D3 [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
Complete structured claim and evidenceThe CaSR E128A variant increases receptor responsiveness and causes dominant hypocalcemia in the studied family.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human family; E128A CaSR expressed in Xenopus oocytes
- limitations
- One family and oocyte assays; not dietary calcium deficiency.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- An oversensitive sensor can lower blood calcium.
- primary_references
- [pollak1994] Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation (1994). https://pubmed.ncbi.nlm.nih.gov/7874174/ DOI: 10.1038/ng1194-303
- tissue_or_cell_type
- Systemic calcium regulation
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 47–56
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family; E128A CaSR expressed in Xenopus oocytes · source_derived_draft · unverified_draft
### casr-gain-hypocalcemia The CaSR E128A variant increases receptor responsiveness and causes dominant hypocalcemia in the studied family. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An oversensitive sensor can lower blood calcium. organism: Homo sapiens tissue_or_cell_type: Systemic calcium regulation experimental_model: Human family; E128A CaSR expressed in Xenopus oocytes limitations: One family and oocyte assays; not dietary calcium deficiency. [pollak1994] Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation (1994). https://pubmed.ncbi.nlm.nih.gov/7874174/ DOI: 10.1038/ng1194-303
Complete structured claim and evidenceInactivating CASR variants cause familial hypocalciuric hypercalcemia or neonatal severe hyperparathyroidism.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human pedigrees and mutant-receptor expression in Xenopus oocytes
- limitations
- Mutation-specific inherited disease; not evidence of dietary calcium excess.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- A faulty sensor can raise blood calcium.
- primary_references
- [pollak1993] Mutations in the human Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism (1993). https://pubmed.ncbi.nlm.nih.gov/7916660/ DOI: 10.1016/0092-8674(93)90617-y
- tissue_or_cell_type
- Parathyroid/kidney calcium regulation
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 36–45
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pedigrees and mutant-receptor expression in Xenopus oocytes · source_derived_draft · unverified_draft
### casr-loss-hypercalcemia Inactivating CASR variants cause familial hypocalciuric hypercalcemia or neonatal severe hyperparathyroidism. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A faulty sensor can raise blood calcium. organism: Homo sapiens tissue_or_cell_type: Parathyroid/kidney calcium regulation experimental_model: Human pedigrees and mutant-receptor expression in Xenopus oocytes limitations: Mutation-specific inherited disease; not evidence of dietary calcium excess. [pollak1993] Mutations in the human Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism (1993). https://pubmed.ncbi.nlm.nih.gov/7916660/ DOI: 10.1016/0092-8674(93)90617-y
Complete structured claim and evidenceVDR-ablated mice develop hypocalcemia around postnatal day 21 with rising PTH.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Mice with targeted disruption of the VDR DNA-binding domain
- limitations
- Global receptor deletion; not isolated dietary calcium shortage.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Mus musculus
- plain_language
- Vitamin D receptor failure disrupts calcium regulation.
- primary_references
- [li1997] Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC23277/ DOI: 10.1073/pnas.94.18.9831
- tissue_or_cell_type
- Systemic mineral metabolism
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Calcium: mechanism-first literature curation (2026-09-17) · lines 135–144
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice with targeted disruption of the VDR DNA-binding domain · source_derived_draft · unverified_draft
### vdr-loss-hypocalcemia VDR-ablated mice develop hypocalcemia around postnatal day 21 with rising PTH. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin D receptor failure disrupts calcium regulation. organism: Mus musculus tissue_or_cell_type: Systemic mineral metabolism experimental_model: Mice with targeted disruption of the VDR DNA-binding domain limitations: Global receptor deletion; not isolated dietary calcium shortage. [li1997] Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC23277/ DOI: 10.1073/pnas.94.18.9831
Complete structured claim and evidenceRetinyl palmitate attenuated the serum-calcium rise after calcitriol in the small crossover.
Experimental context and source evidence
- cross_nutrient
- Retinyl ester/calcitriol/calcium interaction.
- experimental_model
- Nine adults; acute blinded crossover.
- exposure
- 15 mg retinyl palmitate and/or 2 micrograms calcitriol; historical experiment, not advice.
- limitations
- Serum response is not a direct isotope absorption measurement, long-term fracture outcome or universal vitamin A:D ratio.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens
- plain_language
- Vitamin A form and exposure changed a measured vitamin D/calcium response.
- primary_references
- [va-johansson2001] Vitamin A antagonizes calcium response to vitamin D in man (2001). https://pubmed.ncbi.nlm.nih.gov/11585356/ DOI: 10.1359/jbmr.2001.16.10.1899
- tissue_or_cell_type
- Serum
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1601–1612
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Nine adults; acute blinded crossover. · source_derived_draft · unverified_draft
### va-retinyl-palmitate-calcitriol-calcium Retinyl palmitate attenuated the serum-calcium rise after calcitriol in the small crossover. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A form and exposure changed a measured vitamin D/calcium response. organism: Homo sapiens tissue_or_cell_type: Serum experimental_model: Nine adults; acute blinded crossover. limitations: Serum response is not a direct isotope absorption measurement, long-term fracture outcome or universal vitamin A:D ratio. cross_nutrient: Retinyl ester/calcitriol/calcium interaction. exposure: 15 mg retinyl palmitate and/or 2 micrograms calcitriol; historical experiment, not advice. [va-johansson2001] Vitamin A antagonizes calcium response to vitamin D in man (2001). https://pubmed.ncbi.nlm.nih.gov/11585356/ DOI: 10.1359/jbmr.2001.16.10.1899
Complete structured claim and evidenceThe ferric-carboxymaltose substudy found lower calcium accompanying the intact-FGF23 rise.
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
- Calcium regulation was affected along with phosphate.
- 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 1024–1035
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-calcium The ferric-carboxymaltose substudy found lower calcium accompanying the intact-FGF23 rise. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium regulation was affected along with phosphate. 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 evidence
Where it participates (unsigned role)
Mg biomarkers declined on the low-Mg diet, but hypomagnesemia, hypocalcemia and hypokalemia were not detected.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence-system
- Crossover feeding and biochemical monitoring
- experimental_model
- Crossover feeding and biochemical monitoring
- exposure
- Chemically measured mean intake: 130 mg Mg/day in the low period versus 411 mg/day in the supplemented period; 81 days per period after 10-day equilibration. These are experimental exposures, not recommendations.
- limitations
- A study-specific biomarker observation; not a diagnostic rule for all normal serum values.
- nutrient_topic
- Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
- organism
- Human
- plain_language
- A normal-range serum result did not rule out the diet-related electrical phenotype in these participants.
- primary_references
- [klevay-2002-ectopy] Low dietary magnesium increases supraventricular ectopy (2002). https://ajcn.nutrition.org/article/S0002-9165%2823%2906154-3/fulltext DOI: 10.1093/ajcn/75.3.550
- tissue
- Serum, erythrocytes and urine
- tissue_or_cell_type
- Serum, erythrocytes and urine
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1332–1344
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crossover feeding and biochemical monitoring · source_derived_draft · unverified_draft
### low-magnesium-diet-without-hypomagnesemia Mg biomarkers declined on the low-Mg diet, but hypomagnesemia, hypocalcemia and hypokalemia were not detected. Condition category: biomarker_context nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A normal-range serum result did not rule out the diet-related electrical phenotype in these participants. organism: Human tissue_or_cell_type: Serum, erythrocytes and urine experimental_model: Crossover feeding and biochemical monitoring limitations: A study-specific biomarker observation; not a diagnostic rule for all normal serum values. exposure: Chemically measured mean intake: 130 mg Mg/day in the low period versus 411 mg/day in the supplemented period; 81 days per period after 10-day equilibration. These are experimental exposures, not recommendations. evidence-system: Crossover feeding and biochemical monitoring tissue: Serum, erythrocytes and urine [klevay-2002-ectopy] Low dietary magnesium increases supraventricular ectopy (2002). https://ajcn.nutrition.org/article/S0002-9165%2823%2906154-3/fulltext DOI: 10.1093/ajcn/75.3.550
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 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.