Component
Sodium chloride
Independent biological entity. Read linked claims for experimental scope and context.
15 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
Higher salt shifted modeled bone calcium balance from positive to negative on the higher-calcium diet; balance was negative at both salt levels on the lower-calcium diet.
Experimental context and source evidence
- 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
- Calcium intake changed the context of the modeled salt effect; this was not a fracture trial.
- 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 1123–1134
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-bone-model Higher salt shifted modeled bone calcium balance from positive to negative on the higher-calcium diet; balance was negative at both salt levels on the lower-calcium diet. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium intake changed the context of the modeled salt effect; this was not a fracture trial. 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
Complete structured claim and evidenceFractional calcium absorption adapted to calcium intake but was not significantly altered by salt intake.
Experimental context and source evidence
- 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
- The kidney calcium loss was not matched by a measured salt-driven increase in absorption.
- 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 1110–1121
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-calcium-absorption Fractional calcium absorption adapted to calcium intake but was not significantly altered by salt intake. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney calcium loss was not matched by a measured salt-driven increase in absorption. 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
Complete structured claim and evidenceThe higher-salt diet increased urinary calcium excretion in the crossover trial (P=0.0008).
Experimental context and source evidence
- 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
Complete structured claim and evidenceFluid intake was lower at 12 g/day salt in these long-duration controlled studies.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"}
- experimental_model
- Two controlled confinement studies lasting 105 and 205 days, totaling 10 men
- exposure
- 6, 9 and 12 g/day salt; other nutrients held constant
- limitations
- Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human healthy men
- plain_language
- Long-term fluid behavior in this setting did not follow a simple more-salt–more-drinking rule.
- primary_references
- [sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
- tissue_or_cell_type
- Whole-body water and osmolyte balance
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1149–1160
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two controlled confinement studies lasting 105 and 205 days, totaling 10 men · source_derived_draft · unverified_draft
### sodium-salt-drinking Fluid intake was lower at 12 g/day salt in these long-duration controlled studies. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Long-term fluid behavior in this setting did not follow a simple more-salt–more-drinking rule. organism: Human healthy men tissue_or_cell_type: Whole-body water and osmolyte balance experimental_model: Two controlled confinement studies lasting 105 and 205 days, totaling 10 men limitations: Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects. exposure: 6, 9 and 12 g/day salt; other nutrients held constant evidence_span: {"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"} [sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
Complete structured claim and evidenceMice fed a high-salt diet developed more severe experimental autoimmune encephalomyelitis.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
- experimental_model
- Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
- exposure
- Increased NaCl in culture or high-salt mouse diet
- limitations
- NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human and mouse T cells; mouse disease model
- plain_language
- The cell findings had a disease-model counterpart in mice; human disease causation remains unproven.
- primary_references
- [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
- tissue_or_cell_type
- T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 538–549
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-salt-eae Mice fed a high-salt diet developed more severe experimental autoimmune encephalomyelitis. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell findings had a disease-model counterpart in mice; human disease causation remains unproven. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidenceModestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
- experimental_model
- T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
- exposure
- NaCl elevation and Sgk1 perturbation
- limitations
- The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Mouse
- plain_language
- Salt exposure can reinforce responsiveness to an immune signal in this model.
- primary_references
- [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
- tissue_or_cell_type
- IL-23-responsive TH17 cells
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 577–588
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft
### sodium-salt-il23r Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Salt exposure can reinforce responsiveness to an immune signal in this model. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
Complete structured claim and evidenceIncreased NaCl enhanced cytokine-induced TH17 differentiation in human and mouse T-cell cultures.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
- experimental_model
- Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
- exposure
- Increased NaCl in culture or high-salt mouse diet
- limitations
- NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human and mouse T cells; mouse disease model
- plain_language
- Salt conditions can change immune-cell differentiation in an experimental setting.
- primary_references
- [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
- tissue_or_cell_type
- T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 486–497
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-salt-th17 Increased NaCl enhanced cytokine-induced TH17 differentiation in human and mouse T-cell cultures. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Salt conditions can change immune-cell differentiation in an experimental setting. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidenceThe 6-g/day salt increase reduced free-water clearance while increasing urine osmolyte excretion.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"}
- experimental_model
- Two controlled confinement studies lasting 105 and 205 days, totaling 10 men
- exposure
- 6, 9 and 12 g/day salt; other nutrients held constant
- limitations
- Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human healthy men
- plain_language
- The kidneys adjusted water conservation during sustained salt exposure.
- primary_references
- [sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
- tissue_or_cell_type
- Whole-body water and osmolyte balance
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 1136–1147
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two controlled confinement studies lasting 105 and 205 days, totaling 10 men · source_derived_draft · unverified_draft
### sodium-salt-water-clearance The 6-g/day salt increase reduced free-water clearance while increasing urine osmolyte excretion. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidneys adjusted water conservation during sustained salt exposure. organism: Human healthy men tissue_or_cell_type: Whole-body water and osmolyte balance experimental_model: Two controlled confinement studies lasting 105 and 205 days, totaling 10 men limitations: Small all-male long-duration study; reduced free-water clearance is not creation of water. Do not extrapolate to acute salt ingestion, all populations or immune effects. exposure: 6, 9 and 12 g/day salt; other nutrients held constant evidence_span: {"source_cache": "artifacts/sodium-research/28414302.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d", "start_char": 0, "end_char": 2118, "text_sha256": "099d2bd468b387701a756371dde0732e2eba2b5d15d02948a99fc96c3df3046d"} [sodium-p28414302] Increased salt consumption induces body water conservation and decreases fluid intake. (2017). https://pubmed.ncbi.nlm.nih.gov/28414302/ DOI: 10.1172/jci88530
Complete structured claim and evidence
Where it participates (unsigned role)
Silencing or chemical inhibition of NFAT5 blocked the high-salt enhancement of TH17 differentiation in the study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
- experimental_model
- Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
- exposure
- Increased NaCl in culture or high-salt mouse diet
- limitations
- NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human and mouse T cells; mouse disease model
- plain_language
- Blocking NFAT5 interrupted this particular salt-sensitive immune response.
- primary_references
- [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
- tissue_or_cell_type
- T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 512–523
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-th17-nfat5 Silencing or chemical inhibition of NFAT5 blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking NFAT5 interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidenceSilencing or chemical inhibition of p38/MAPK blocked the high-salt enhancement of TH17 differentiation in the study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
- experimental_model
- Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
- exposure
- Increased NaCl in culture or high-salt mouse diet
- limitations
- NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human and mouse T cells; mouse disease model
- plain_language
- Blocking p38/MAPK interrupted this particular salt-sensitive immune response.
- primary_references
- [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
- tissue_or_cell_type
- T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 499–510
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-th17-p38 Silencing or chemical inhibition of p38/MAPK blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking p38/MAPK interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidenceSilencing or chemical inhibition of SGK1 blocked the high-salt enhancement of TH17 differentiation in the study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
- experimental_model
- Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
- exposure
- Increased NaCl in culture or high-salt mouse diet
- limitations
- NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human and mouse T cells; mouse disease model
- plain_language
- Blocking SGK1 interrupted this particular salt-sensitive immune response.
- primary_references
- [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
- tissue_or_cell_type
- T-helper cells and experimental CNS autoimmunity
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 525–536
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft
### sodium-th17-sgk1 Silencing or chemical inhibition of SGK1 blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking SGK1 interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
Complete structured claim and evidencePotassium chloride and sodium chloride increased home systolic pressure versus placebo in the CKD crossover.
Experimental context and source evidence
- cross_nutrient
- Chloride salt/kidney context -> pressure.
- experimental_model
- Same five-day periods.
- limitations
- Context difference, not proof of a universal adverse potassium effect; molecular mediator unproven.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Homo sapiens
- plain_language
- The pressure response differed from trials in people with better kidney function.
- primary_references
- [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
- tissue_or_cell_type
- Systemic circulation
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1685–1695
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same five-day periods. · source_derived_draft · unverified_draft
### k-ckd-chloride-salt-pressure Potassium chloride and sodium chloride increased home systolic pressure versus placebo in the CKD crossover. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pressure response differed from trials in people with better kidney function. organism: Homo sapiens tissue_or_cell_type: Systemic circulation experimental_model: Same five-day periods. limitations: Context difference, not proof of a universal adverse potassium effect; molecular mediator unproven. cross_nutrient: Chloride salt/kidney context -> pressure. [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
Complete structured claim and evidenceThe 75% NaCl/25% KCl salt substitute reduced stroke incidence versus ordinary salt in SSaSS (rate ratio 0.86).
Experimental context and source evidence
- cross_nutrient
- Combined sodium reduction/potassium increase; not potassium-alone molecular causation.
- experimental_model
- Cluster-randomized trial; mean 4.74-year follow-up.
- limitations
- Both sodium and potassium changed, so their effects cannot be separated. Serious kidney disease and potassium-sparing drugs/supplements were excluded; no serial serum-potassium surveillance.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Homo sapiens
- plain_language
- Replacing part of sodium chloride with potassium chloride improved a clinical outcome in the studied population.
- primary_references
- [k-neal2021] Effect of Salt Substitution on Cardiovascular Events and Death (2021). https://pubmed.ncbi.nlm.nih.gov/34459569/ DOI: 10.1056/nejmoa2105675
- tissue_or_cell_type
- Clinical cerebrovascular outcome
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1697–1707
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cluster-randomized trial; mean 4.74-year follow-up. · source_derived_draft · unverified_draft
### k-sodium-potassium-salt-stroke-trial The 75% NaCl/25% KCl salt substitute reduced stroke incidence versus ordinary salt in SSaSS (rate ratio 0.86). Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing part of sodium chloride with potassium chloride improved a clinical outcome in the studied population. organism: Homo sapiens tissue_or_cell_type: Clinical cerebrovascular outcome experimental_model: Cluster-randomized trial; mean 4.74-year follow-up. limitations: Both sodium and potassium changed, so their effects cannot be separated. Serious kidney disease and potassium-sparing drugs/supplements were excluded; no serial serum-potassium surveillance. cross_nutrient: Combined sodium reduction/potassium increase; not potassium-alone molecular causation. [k-neal2021] Effect of Salt Substitution on Cardiovascular Events and Death (2021). https://pubmed.ncbi.nlm.nih.gov/34459569/ DOI: 10.1056/nejmoa2105675
Complete structured claim and evidenceMSG is the sodium salt of L-glutamate; the sensory study treats added MSG and NaCl as separate ingredients.
Experimental context and source evidence
- evidence_access
- Primary full text; background and test samples
- experimental_model
- Chemical identity and ingredient design in the primary sensory study.
- limitations
- This is background chemistry, not a measurement of absorption or tissue delivery.
- nutrient_topic
- Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
- plain_language
- The ingredient contributes both glutamate and sodium.
- primary_references
- Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 18–24
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Chemical identity and ingredient design in the primary sensory study. · source_derived_draft · unverified_draft
## monosodium-glutamate-salt-identity The ingredient contributes both glutamate and sodium. MSG is the sodium salt of L-glutamate; the sensory study treats added MSG and NaCl as separate ingredients. Model: Chemical identity and ingredient design in the primary sensory study. Limitations: This is background chemistry, not a measurement of absorption or tissue delivery. Evidence access: Primary full text; background and test samples Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
Complete structured claim and evidenceIn 584 participants, adding 0.3% MSG improved palatability ratings at tested 0.3%, 0.6% and 0.9% NaCl concentrations.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Randomized blinded tasting across nineteen Japanese regions.
- limitations
- MSG itself adds sodium; net reduction requires NaCl replacement. No long-term sodium intake or blood-pressure effect was measured. Three authors were Ajinomoto employees.
- nutrient_topic
- Monosodium Glutamate (MSG) collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Monosodium L-glutamate
- plain_language
- Flavor enhancement may help a lower-salt recipe remain acceptable.
- primary_references
- Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
Monosodium Glutamate (MSG): taste, gut sensing, exposure and cross-nutrient mechanisms (2026-09-20) · lines 250–256
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized blinded tasting across nineteen Japanese regions. · source_derived_draft · unverified_draft
## monosodium-glutamate-sodium-substitution Flavor enhancement may help a lower-salt recipe remain acceptable. In 584 participants, adding 0.3% MSG improved palatability ratings at tested 0.3%, 0.6% and 0.9% NaCl concentrations. Model: Randomized blinded tasting across nineteen Japanese regions. Limitations: MSG itself adds sodium; net reduction requires NaCl replacement. No long-term sodium intake or blood-pressure effect was measured. Three authors were Ajinomoto employees. Evidence access: Primary full text Validation of preferred salt concentration in soup based on a randomized blinded experiment in multiple regions in Japan-influence of umami (L-glutamate) on saltiness and palatability of low-salt solutions. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31996813/ · DOI 10.1038/s41440-020-0397-1
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.