Urinary calcium excretion

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}

experimental_model

Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria

exposure

SLC34A3 disease-associated mutations in five families

limitations

Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.

nutrient_topic

Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium

organism

Human

plain_language

This phosphate disorder can also increase calcium loss into urine.

primary_references

[sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410

tissue_or_cell_type

Renal proximal tubule and systemic mineral phenotype

trigger_kind

machinery_impairment Imported condition classification; unverified.

Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 694–705

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft

### sodium-napi2c-calcium The sodium/phosphate-transporter-associated HHRH phenotype included hypercalciuria. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This phosphate disorder can also increase calcium loss into urine. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410

evidence_span

{"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"}

experimental_model

Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers

exposure

Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily

limitations

Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium.

nutrient_topic

Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium

organism

Human postmenopausal women

plain_language

More dietary salt increased measured urinary calcium loss in these women.

primary_references

[sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408

tissue_or_cell_type

Intestinal, renal and modeled skeletal calcium balance

Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1097–1108

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers · source_derived_draft · unverified_draft

### sodium-salt-calciuria The higher-salt diet increased urinary calcium excretion in the crossover trial (P=0.0008). Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More dietary salt increased measured urinary calcium loss in these women. organism: Human postmenopausal women tissue_or_cell_type: Intestinal, renal and modeled skeletal calcium balance experimental_model: Randomized crossover with stable-isotope calcium measures and compartmental modeling in 11 completers limitations: Small study; bone balance was modeled, fractures were not measured. Salt means sodium chloride, not elemental sodium. exposure: Four five-week calcium/salt diet combinations: 518 or 1284 mg calcium; 3.9 or 11.2 g salt daily evidence_span: {"source_cache": "artifacts/sodium-research/18410231.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa", "start_char": 0, "end_char": 1558, "text_sha256": "f831f038a6c4249510bbeeae68778a216f1c36aa440e33816072959d1a07fefa"} [sodium-p18410231] Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women. (2008). https://pubmed.ncbi.nlm.nih.gov/18410231/ DOI: 10.1359/jbmr.080408

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Human affected families; linkage, sequencing and claudin trafficking/assembly assays

limitations

Multimineral genetic disorder; ocular and renal manifestations vary.

nutrient_topic

Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium

organism

Homo sapiens

plain_language

Inherited junction defects can waste calcium.

primary_references

[konrad2006] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1698561/ DOI: 10.1086/508617

tissue_or_cell_type

Kidney tubules

trigger_kind

machinery_impairment Imported condition classification; unverified.

Calcium: mechanism-first literature curation (2026-09-17) · lines 269–278

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human affected families; linkage, sequencing and claudin trafficking/assembly assays · source_derived_draft · unverified_draft

### cldn19-variants-renal-calcium-wasting Biallelic CLDN19 variants were identified in families with renal magnesium wasting, hypercalciuria and nephrocalcinosis. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited junction defects can waste calcium. organism: Homo sapiens tissue_or_cell_type: Kidney tubules experimental_model: Human affected families; linkage, sequencing and claudin trafficking/assembly assays limitations: Multimineral genetic disorder; ocular and renal manifestations vary. [konrad2006] Mutations in the tight-junction gene claudin 19 (CLDN19) are associated with renal magnesium wasting, renal failure, and severe ocular involvement (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1698561/ DOI: 10.1086/508617

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models

limitations

Global deletion also affects intestinal handling.

nutrient_topic

Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium

organism

Mus musculus

plain_language

The two claudins provide complementary renal retention.

primary_references

[beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118

tissue_or_cell_type

Kidney; proximal-tubule localization

trigger_kind

machinery_impairment Imported condition classification; unverified.

Calcium: mechanism-first literature curation (2026-09-17) · lines 225–234

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models · source_derived_draft · unverified_draft

### cldn2-cldn12-double-loss-calciuria Cldn2/Cldn12 double-null mice lose more urinary calcium than Cldn2-null mice. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two claudins provide complementary renal retention. organism: Mus musculus tissue_or_cell_type: Kidney; proximal-tubule localization experimental_model: Cldn2/Cldn12 single/double knockout mice, ex vivo epithelia and cell models limitations: Global deletion also affects intestinal handling. [beggs2021] Claudin-2 and claudin-12 form independent, complementary pores required to maintain calcium homeostasis (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8694054/ DOI: 10.1073/pnas.2111247118

cross_nutrient

Bicarbonate coadministration modifies the calcium response attributed to potassium salts.

endpoint

The bicarbonate-containing arms reduced calcium excretion relative to non-bicarbonate arms in the older-adult trial; a potassium main effect was not significant.

experimental-exposure

171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D.

experimental_model

171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D.

limitations

Pooled factorial comparison, calcium/vitamin D co-supplementation, three-month surrogate endpoint; not evidence of fracture prevention or universal potassium neutrality.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

The calcium-loss effect tracked the alkali component rather than the presence of potassium in the salt.

primary_references

[dawson-hughes-2009-bicarbonate] Treatment with Potassium Bicarbonate Lowers Calcium Excretion and Bone Resorption in Older Men and Women (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2630872/ DOI: 10.1210/jc.2008-1662

tissue_or_cell_type

kidney and urine

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1260–1272

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D. · source_derived_draft · unverified_draft

### bicarbonate-component-lowers-calciuria The bicarbonate-containing arms reduced calcium excretion relative to non-bicarbonate arms in the older-adult trial; a potassium main effect was not significant. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The calcium-loss effect tracked the alkali component rather than the presence of potassium in the salt. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: 171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D. limitations: Pooled factorial comparison, calcium/vitamin D co-supplementation, three-month surrogate endpoint; not evidence of fracture prevention or universal potassium neutrality. cross_nutrient: Bicarbonate coadministration modifies the calcium response attributed to potassium salts. experimental-exposure: 171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D. endpoint: The bicarbonate-containing arms reduced calcium excretion relative to non-bicarbonate arms in the older-adult trial; a potassium main effect was not significant. [dawson-hughes-2009-bicarbonate] Treatment with Potassium Bicarbonate Lowers Calcium Excretion and Bone Resorption in Older Men and Women (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2630872/ DOI: 10.1210/jc.2008-1662

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium deprivation increases renal calcium loss in a controlled human dietary model.

endpoint

Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3.

experimental-exposure

Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four.

experimental_model

Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four.

limitations

Small controlled metabolic study; sodium balance, extracellular volume, phosphate handling and calcitriol were possible mediators rather than proven causal links.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

Potassium deprivation changed calcium retention even when alkali withdrawal was not the only explanation.

primary_references

[lemann-1991-calciuria] Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected] (1991). https://pubmed.ncbi.nlm.nih.gov/1648646/ DOI: 10.1038/ki.1991.123

tissue_or_cell_type

kidney and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1274–1286

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. · source_derived_draft · unverified_draft

### human-k-withdrawal-increases-calciuria Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium deprivation changed calcium retention even when alkali withdrawal was not the only explanation. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. limitations: Small controlled metabolic study; sodium balance, extracellular volume, phosphate handling and calcitriol were possible mediators rather than proven causal links. cross_nutrient: Potassium deprivation increases renal calcium loss in a controlled human dietary model. experimental-exposure: Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. endpoint: Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3. [lemann-1991-calciuria] Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected] (1991). https://pubmed.ncbi.nlm.nih.gov/1648646/ DOI: 10.1038/ki.1991.123

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.

endpoint

Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments.

experimental-exposure

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

experimental_model

Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.

limitations

Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Mus musculus

plain_language

The kidneys lost more calcium when dietary potassium was restricted.

primary_references

[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

tissue_or_cell_type

kidney, blood and trabecular skeleton

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1288–1300

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft

### mouse-k-restriction-calciuria Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidneys lost more calcium when dietary potassium was restricted. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Low K increases urinary calcium output under the tested sodium background.

evidence_location

Primary abstract; final-week balance results.

experimental_model

Four-week 0.2% versus 4% K diet; both 8% NaCl

limitations

Weanling males; unusual salt/mineral diets; causal transport site and BP mediation unproven.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Rattus norvegicus

plain_language

In this high-salt setting, lower potassium intake increased calcium loss in urine.

primary_references

[wu-1995-k-calcium] Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions (1995). https://pubmed.ncbi.nlm.nih.gov/7581265/ DOI: 10.3109/10641969509033647

tissue_or_cell_type

Kidney/urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 510–521

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week 0.2% versus 4% K diet; both 8% NaCl · source_derived_draft · unverified_draft

### renal-low-k-increases-calcium-loss-high-salt Low versus high dietary K increased calcium excretion in both salt-sensitive and salt-resistant Dahl rats on high NaCl. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this high-salt setting, lower potassium intake increased calcium loss in urine. organism: Rattus norvegicus tissue_or_cell_type: Kidney/urine experimental_model: Four-week 0.2% versus 4% K diet; both 8% NaCl limitations: Weanling males; unusual salt/mineral diets; causal transport site and BP mediation unproven. cross_nutrient: Low K increases urinary calcium output under the tested sodium background. evidence_location: Primary abstract; final-week balance results. [wu-1995-k-calcium] Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions (1995). https://pubmed.ncbi.nlm.nih.gov/7581265/ DOI: 10.3109/10641969509033647

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/boron-research/9062533.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a23cd1fe09277bdd83b690746d4bbaf4742cdd74e51d5b27ee898bd87208b2be", "start_char": 0, "end_char": 1720, "text_sha256": "a23cd1fe09277bdd83b690746d4bbaf4742cdd74e51d5b27ee898bd87208b2be"}

experimental_model

Metabolic-ward feeding; 11 postmenopausal volunteers

exposure

167-day study; basal 0.36 mg B and 109 mg Mg/8400 kJ; 3 mg/day B supplement in last two 24-day periods; magnesium supplement 0 or 200 mg/day

limitations

Small study with multiple dietary periods and supplements. Do not assume independence from related reports from the same research program. Urine composition is not a kidney-stone clinical endpoint.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Human

plain_language

The calcium response changed direction with the magnesium diet.

primary_references

[boron-p9062533] Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations. (1997). https://pubmed.ncbi.nlm.nih.gov/9062533/ DOI: 10.1093/ajcn/65.3.803

tissue_or_cell_type

Mineral balance, blood and excreta

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 664–675

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolic-ward feeding; 11 postmenopausal volunteers · source_derived_draft · unverified_draft

### boron-calcium-magnesium-context-1997 Boron supplementation lowered the fraction of dietary calcium excreted in urine under basal magnesium intake but increased that fraction with magnesium supplementation. Condition category: nutrient_deficiency nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The calcium response changed direction with the magnesium diet. organism: Human tissue_or_cell_type: Mineral balance, blood and excreta experimental_model: Metabolic-ward feeding; 11 postmenopausal volunteers limitations: Small study with multiple dietary periods and supplements. Do not assume independence from related reports from the same research program. Urine composition is not a kidney-stone clinical endpoint. exposure: 167-day study; basal 0.36 mg B and 109 mg Mg/8400 kJ; 3 mg/day B supplement in last two 24-day periods; magnesium supplement 0 or 200 mg/day evidence_span: {"source_cache": "artifacts/boron-research/9062533.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a23cd1fe09277bdd83b690746d4bbaf4742cdd74e51d5b27ee898bd87208b2be", "start_char": 0, "end_char": 1720, "text_sha256": "a23cd1fe09277bdd83b690746d4bbaf4742cdd74e51d5b27ee898bd87208b2be"} [boron-p9062533] Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations. (1997). https://pubmed.ncbi.nlm.nih.gov/9062533/ DOI: 10.1093/ajcn/65.3.803

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/boron-research/8329361.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e6e2137f75699ea6dce582375f335a85139fea1cfa7ec502f033e8bfe026d63", "start_char": 0, "end_char": 1079, "text_sha256": "3e6e2137f75699ea6dce582375f335a85139fea1cfa7ec502f033e8bfe026d63"}

experimental_model

Metabolic-unit low-intake/supplementation follow-up

exposure

0.33 mg boron/day for three weeks, then an additional 3 mg/day for three weeks

limitations

Small, short sequential study. The background diet produced positive calcium balance with increased urinary calcium; the authors proposed that this could mask a boron effect, but did not prove the explanation.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Human postmenopausal volunteers

plain_language

This follow-up did not reproduce the earlier calcium-sparing finding.

primary_references

[boron-p8329361] The influence of a low-boron diet and boron supplementation on bone, major mineral and sex steroid metabolism in postmenopausal women. (1993). https://pubmed.ncbi.nlm.nih.gov/8329361/ DOI: 10.1079/bjn19930087

tissue_or_cell_type

Mineral balance, hormones and bone-turnover markers

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 703–714

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metabolic-unit low-intake/supplementation follow-up · source_derived_draft · unverified_draft

### boron-human-calcium-null-1993 Increasing boron intake from 0.33 to 3.33 mg/day did not alter the measured mineral absorption or excretion endpoints in the 1993 follow-up study. Condition category: nutrient_deficiency nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: This follow-up did not reproduce the earlier calcium-sparing finding. organism: Human postmenopausal volunteers tissue_or_cell_type: Mineral balance, hormones and bone-turnover markers experimental_model: Metabolic-unit low-intake/supplementation follow-up limitations: Small, short sequential study. The background diet produced positive calcium balance with increased urinary calcium; the authors proposed that this could mask a boron effect, but did not prove the explanation. exposure: 0.33 mg boron/day for three weeks, then an additional 3 mg/day for three weeks evidence_span: {"source_cache": "artifacts/boron-research/8329361.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3e6e2137f75699ea6dce582375f335a85139fea1cfa7ec502f033e8bfe026d63", "start_char": 0, "end_char": 1079, "text_sha256": "3e6e2137f75699ea6dce582375f335a85139fea1cfa7ec502f033e8bfe026d63"} [boron-p8329361] The influence of a low-boron diet and boron supplementation on bone, major mineral and sex steroid metabolism in postmenopausal women. (1993). https://pubmed.ncbi.nlm.nih.gov/8329361/ DOI: 10.1079/bjn19930087

availability_state

nutrient_deficiency Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/boron-research/3678698.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7", "start_char": 0, "end_char": 1373, "text_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7"}

experimental_model

Sequential controlled feeding in a metabolic unit; 12 postmenopausal women

exposure

About 0.25 mg boron/day for 119 days, then 3 mg/day supplement; seven low-magnesium and five adequate-magnesium participants

limitations

Small sequential study, not a fracture or bone-density trial. Diet and magnesium status matter. Later studies did not consistently reproduce the reported effects.

nutrient_topic

Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron

organism

Human

plain_language

The women lost less calcium in urine under this particular feeding regimen.

primary_references

[boron-p3678698] Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. (1987). https://pubmed.ncbi.nlm.nih.gov/3678698/ DOI: 10.1096/fasebj.1.5.3678698

tissue_or_cell_type

Systemic mineral balance and circulating hormones

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 599–610

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Sequential controlled feeding in a metabolic unit; 12 postmenopausal women · source_derived_draft · unverified_draft

### boron-human-calcium-sparing-1987 A 3 mg/day boron supplement after prolonged low intake reduced urinary calcium in the 1987 postmenopausal feeding study, apparently more strongly with low magnesium intake. Condition category: nutrient_deficiency nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The women lost less calcium in urine under this particular feeding regimen. organism: Human tissue_or_cell_type: Systemic mineral balance and circulating hormones experimental_model: Sequential controlled feeding in a metabolic unit; 12 postmenopausal women limitations: Small sequential study, not a fracture or bone-density trial. Diet and magnesium status matter. Later studies did not consistently reproduce the reported effects. exposure: About 0.25 mg boron/day for 119 days, then 3 mg/day supplement; seven low-magnesium and five adequate-magnesium participants evidence_span: {"source_cache": "artifacts/boron-research/3678698.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7", "start_char": 0, "end_char": 1373, "text_sha256": "8f95ac01b63502b366e2bd79785b7203deb793d258df065f13cc1e0123c89fb7"} [boron-p3678698] Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. (1987). https://pubmed.ncbi.nlm.nih.gov/3678698/ DOI: 10.1096/fasebj.1.5.3678698

experimental_model

Randomized crossover feeding trial in 14 women

limitations

No lysine-only arm or demonstrated long-term calcium-balance effect.

organism

Homo sapiens

plain_language

More urinary calcium accompanied the mixture; it cannot by itself be read as either bone loss or better bone health.

primary_references

[bihuniak2014] Supplementing a low-protein diet with dibasic amino acids increases urinary calcium excretion in young women (2014). https://pmc.ncbi.nlm.nih.gov/articles/PMC3927545/ DOI: 10.3945/jn.113.185009

tissue_or_cell_type

Kidney and urine

L-Lysine: mechanism-first literature curation (2026-09-17) · lines 779–787

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover feeding trial in 14 women · source_derived_draft · unverified_draft

### dibasic-urinary-calcium-increase In the same crossover study, lysine plus arginine significantly increased urinary calcium compared with the low-protein control diet. Plain language: More urinary calcium accompanied the mixture; it cannot by itself be read as either bone loss or better bone health. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Kidney and urine experimental_model: Randomized crossover feeding trial in 14 women limitations: No lysine-only arm or demonstrated long-term calcium-balance effect. [bihuniak2014] Supplementing a low-protein diet with dibasic amino acids increases urinary calcium excretion in young women (2014). https://pmc.ncbi.nlm.nih.gov/articles/PMC3927545/ DOI: 10.3945/jn.113.185009

experimental_model

Acute calcium-load comparison; healthy and osteoporotic women

limitations

Acute load response does not establish long-term calcium balance or skeletal outcomes.

organism

Homo sapiens

plain_language

Lysine altered short-term urinary calcium handling in one subgroup.

primary_references

[civitelli1992] Dietary L-lysine and calcium metabolism in humans (1992). https://pubmed.ncbi.nlm.nih.gov/1486246/

tissue_or_cell_type

Kidney and urine

L-Lysine: mechanism-first literature curation (2026-09-17) · lines 759–767

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Acute calcium-load comparison; healthy and osteoporotic women · source_derived_draft · unverified_draft

### lysine-calcium-urinary-blunting In healthy women, adding 400 mg lysine to a calcium load blunted the subsequent rise in urinary calcium; this pattern was not reported for the osteoporotic group. Plain language: Lysine altered short-term urinary calcium handling in one subgroup. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Kidney and urine experimental_model: Acute calcium-load comparison; healthy and osteoporotic women limitations: Acute load response does not establish long-term calcium balance or skeletal outcomes. [civitelli1992] Dietary L-lysine and calcium metabolism in humans (1992). https://pubmed.ncbi.nlm.nih.gov/1486246/

evidence_access

Primary abstract

experimental_model

17 adults; controlled diet; two 3 mg/kg lean-body-mass doses on day two of a before/after metabolic-ward trial.

limitations

Two-day urinary balance is not total body mineral balance or a long-term deficiency diagnosis.

nutrient_topic

Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine

plain_language

Later compensation reduced, but did not erase, the measured daily loss.

primary_references

Effect of caffeine on circadian excretion of urinary calcium and magnesium. · 1994 · https://pubmed.ncbi.nlm.nih.gov/7836625/ · DOI 10.1080/07315724.1994.10718436

Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 340–346

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · 17 adults; controlled diet; two 3 mg/kg lean-body-mass doses on day two of a before/after metabolic-ward trial. · source_derived_draft · unverified_draft

## caf-ca24 Later compensation reduced, but did not erase, the measured daily loss. Later nighttime conservation did not fully offset earlier loss; net 24-hour urinary excretion increased by 0.32 mmol. Model: 17 adults; controlled diet; two 3 mg/kg lean-body-mass doses on day two of a before/after metabolic-ward trial. Limitations: Two-day urinary balance is not total body mineral balance or a long-term deficiency diagnosis. Evidence access: Primary abstract Effect of caffeine on circadian excretion of urinary calcium and magnesium. · 1994 · https://pubmed.ncbi.nlm.nih.gov/7836625/ · DOI 10.1080/07315724.1994.10718436

evidence_access

Primary abstract

experimental_model

37 women, age 31–78; decaffeinated beverage with or without caffeine 6 mg/kg lean body mass; two-hour urine collection.

limitations

Acute renal handling. The exact tubular mechanism was unresolved; no long-term deficiency, bone loss or replacement requirement measured.

nutrient_topic

Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine

plain_language

The acute urine measurement increased.

primary_references

Effects of dietary caffeine on renal handling of minerals in adult women. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2402180/ · DOI 10.1016/0024-3205(90)90616-y

Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 300–306

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · 37 women, age 31–78; decaffeinated beverage with or without caffeine 6 mg/kg lean body mass; two-hour urine collection. · source_derived_draft · unverified_draft

## caf-urine-ca The acute urine measurement increased. Urinary calcium/creatinine rose from 120 to 200 mg/g. Model: 37 women, age 31–78; decaffeinated beverage with or without caffeine 6 mg/kg lean body mass; two-hour urine collection. Limitations: Acute renal handling. The exact tubular mechanism was unresolved; no long-term deficiency, bone loss or replacement requirement measured. Evidence access: Primary abstract Effects of dietary caffeine on renal handling of minerals in adult women. · 1990 · https://pubmed.ncbi.nlm.nih.gov/2402180/ · DOI 10.1016/0024-3205(90)90616-y

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Potassium -> calcium/phosphate/PTH observations.

experimental_model

Concurrent mineral and hormone measurements.

limitations

Co-occurrence does not establish that PTH caused every excretion change.

nutrient_topic

Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium

organism

Homo sapiens

plain_language

Potassium depletion affected calcium-phosphate regulation alongside sodium handling.

primary_references

[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77

tissue_or_cell_type

Plasma and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1534–1544

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Concurrent mineral and hormone measurements. · source_derived_draft · unverified_draft

### k-depletion-human-mineral-pth-response The depletion period also increased urinary calcium and phosphate and plasma immunoreactive PTH. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium depletion affected calcium-phosphate regulation alongside sodium handling. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Concurrent mineral and hormone measurements. limitations: Co-occurrence does not establish that PTH caused every excretion change. cross_nutrient: Potassium -> calcium/phosphate/PTH observations. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77