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.

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.

Recorded relationships

What it acts on

  1. 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

  1. During early Mg repletion, PTH recovered before serum calcium normalized in the serially studied patients.

    Serum PTH concentration → Serum calcium concentration source_derived_draftungraded
    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
  2. Intestinal 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 evidence
  3. Magnesium treatment normalized mean serum calcium, while calcitriol rose into or above normal in only five of the 23 patients.

    Magnesium → Serum calcium concentration source_derived_draftungraded
    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 evidence
  4. A 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 evidence
  5. Three weeks of selective Mg depletion produced a small but significant reduction in serum calcium in the adult study.

    Magnesium → Serum calcium concentration source_derived_draftungraded
    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 evidence
  6. Recessive CYP24A1 variants were identified in infants with hypercalcemia, including a second group whose illness followed high-dose vitamin D prophylaxis.

    Human CYP24A1 gene → Serum calcium concentration source_derived_draftungraded
    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 evidence
  7. The 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 evidence
  8. Inactivating 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 evidence
  9. VDR-ablated mice develop hypocalcemia around postnatal day 21 with rising PTH.

    Vitamin D receptor / VDR → Serum calcium concentration source_derived_draftungraded
    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 evidence
  10. Retinyl 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 evidence
  11. The ferric-carboxymaltose substudy found lower calcium accompanying the intact-FGF23 rise.

    Ferric carboxymaltose → Serum calcium concentration source_derived_draftungraded
    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)

  1. Mg biomarkers declined on the low-Mg diet, but hypomagnesemia, hypocalcemia and hypokalemia were not detected.

    Magnesium → Serum magnesium concentration source_derived_draftungraded
    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 evidence
  2. Most untreated patients in the clinical series had normal or undetectable immunoreactive PTH despite severe hypocalcemia.

    Magnesium → Serum PTH concentration source_derived_draftungraded
    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

In the sources

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    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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