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.

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. 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.

    Sodium chloride → Modeled bone calcium balance source_derived_draftungraded
    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 evidence
  2. Fractional 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 evidence
  3. The higher-salt diet increased urinary calcium excretion in the crossover trial (P=0.0008).

    Sodium chloride → Urinary calcium excretion source_derived_draftungraded
    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 evidence
  4. Fluid intake was lower at 12 g/day salt in these long-duration controlled studies.

    Sodium chloride → Fluid intake source_derived_draftungraded
    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 evidence
  5. Mice 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 evidence
  6. Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program.

    Sodium chloride → Mouse IL-23 receptor expression source_derived_draftungraded
    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 evidence
  7. Increased NaCl enhanced cytokine-induced TH17 differentiation in human and mouse T-cell cultures.

    Sodium chloride → Th17 differentiation source_derived_draftungraded
    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 evidence
  8. The 6-g/day salt increase reduced free-water clearance while increasing urine osmolyte excretion.

    Sodium chloride → Renal free-water clearance source_derived_draftungraded
    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)

  1. 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 evidence
  2. Silencing 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 evidence
  3. Silencing 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 evidence
  4. Potassium chloride and sodium chloride increased home systolic pressure versus placebo in the CKD crossover.

    Potassium chloride → Arterial blood pressure source_derived_draftungraded
    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 evidence
  5. The 75% NaCl/25% KCl salt substitute reduced stroke incidence versus ordinary salt in SSaSS (rate ratio 0.86).

    Potassium chloride → Stroke incidence source_derived_draftungraded
    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 evidence
  6. MSG is the sodium salt of L-glutamate; the sensory study treats added MSG and NaCl as separate ingredients.

    Monosodium L-glutamate → L-Glutamate source_derived_draftungraded
    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 evidence
  7. In 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    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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