Component

Serum magnesium concentration

Measured circulating magnesium concentration; not a direct readout of all tissue stores.

10 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. Low baseline serum magnesium was associated with subsequent refeeding syndrome in the cohort.

    Serum magnesium concentration → Electrolyte and fluid disorder during refeeding source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    experimental_model
    Three syndrome events among 243 adults.
    exposure
    Study-specific exposure described in the model; no regimen inferred beyond the accessed evidence.
    limitations
    Too few events for robust multivariable regression; association does not identify a universal causal bottleneck.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    A mineral shortage was a risk signal alongside poor prior intake.
    primary_references
    [b1-rio2013] Occurrence of refeeding syndrome in adults started on artificial nutrition support: prospective cohort study (2013). https://pubmed.ncbi.nlm.nih.gov/23315514/ DOI: 10.1136/bmjopen-2012-002173
    tissue_or_cell_type
    Serum and clinical course
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1746–1756

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three syndrome events among 243 adults. · source_derived_draft · unverified_draft

    ### b1-refeeding-low-mg-association Low baseline serum magnesium was associated with subsequent refeeding syndrome in the cohort. Condition category: biomarker_context nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A mineral shortage was a risk signal alongside poor prior intake. organism: Homo sapiens tissue_or_cell_type: Serum and clinical course experimental_model: Three syndrome events among 243 adults. limitations: Too few events for robust multivariable regression; association does not identify a universal causal bottleneck. exposure: Study-specific exposure described in the model; no regimen inferred beyond the accessed evidence. [b1-rio2013] Occurrence of refeeding syndrome in adults started on artificial nutrition support: prospective cohort study (2013). https://pubmed.ncbi.nlm.nih.gov/23315514/ DOI: 10.1136/bmjopen-2012-002173
    Complete structured claim and evidence

What acts on it

  1. Pathogenic biallelic TRPM6 variants were identified in families with hypomagnesemia and secondary hypocalcemia.

    TRPM6 loss-of-function genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Calcium concentration also fell in the inherited Mg-handling disorder; this record does not specify the downstream endocrine mechanism.
    evidence-system
    Familial positional genetics
    experimental_model
    Familial positional genetics
    limitations
    Mapping alone does not apportion intestinal versus renal contributions or prove every downstream symptom is Mg-only.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    Inherited failure of magnesium handling produced a recognizable low-magnesium disorder.
    primary_references
    [schlingmann-2002-trpm6] Hypomagnesemia with secondary hypocalcemia is caused by mutations in TRPM6, a new member of the TRPM gene family. (2002). https://pubmed.ncbi.nlm.nih.gov/12032568/ DOI: 10.1038/ng889
    tissue
    Intestine and kidney implicated; serum phenotype
    tissue_or_cell_type
    Intestine and kidney implicated; serum phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 909–921

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Familial positional genetics · source_derived_draft · unverified_draft

    ### human-trpm6-loss-low-magnesium Pathogenic biallelic TRPM6 variants were identified in families with hypomagnesemia and secondary hypocalcemia. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited failure of magnesium handling produced a recognizable low-magnesium disorder. organism: Human tissue_or_cell_type: Intestine and kidney implicated; serum phenotype experimental_model: Familial positional genetics limitations: Mapping alone does not apportion intestinal versus renal contributions or prove every downstream symptom is Mg-only. cross_nutrient: Calcium concentration also fell in the inherited Mg-handling disorder; this record does not specify the downstream endocrine mechanism. evidence-system: Familial positional genetics tissue: Intestine and kidney implicated; serum phenotype [schlingmann-2002-trpm6] Hypomagnesemia with secondary hypocalcemia is caused by mutations in TRPM6, a new member of the TRPM gene family. (2002). https://pubmed.ncbi.nlm.nih.gov/12032568/ DOI: 10.1038/ng889
    Complete structured claim and evidence

  2. Intestine-restricted Trpm6 deletion reduced serum and bone magnesium in the tested adult mice.

    Intestine-specific Trpm6-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Villin1-Cre conditional deletion; six-month-old male mice
    experimental_model
    Villin1-Cre conditional deletion; six-month-old male mice
    limitations
    Colon expression was detected; the outcome does not quantify the contribution of each human intestinal segment.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Removing intestinal TRPM6 impaired systemic magnesium supply despite intact kidneys.
    primary_references
    [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    tissue
    Intestinal epithelium; serum and bone
    tissue_or_cell_type
    Intestinal epithelium; serum and bone
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 923–934

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Villin1-Cre conditional deletion; six-month-old male mice · source_derived_draft · unverified_draft

    ### intestinal-trpm6-loss-low-magnesium Intestine-restricted Trpm6 deletion reduced serum and bone magnesium in the tested adult mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing intestinal TRPM6 impaired systemic magnesium supply despite intact kidneys. organism: Mouse tissue_or_cell_type: Intestinal epithelium; serum and bone experimental_model: Villin1-Cre conditional deletion; six-month-old male mice limitations: Colon expression was detected; the outcome does not quantify the contribution of each human intestinal segment. evidence-system: Villin1-Cre conditional deletion; six-month-old male mice tissue: Intestinal epithelium; serum and bone [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    Complete structured claim and evidence

  3. Intestinal Trpm7 deletion lowered magnesium availability in early postnatal mice.

    Intestine-specific Trpm7-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Villin1-Cre conditional deletion and mineral phenotyping
    experimental_model
    Villin1-Cre conditional deletion and mineral phenotyping
    limitations
    Early developmental model; not a test of dietary Mg restriction.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Suckling mice required intestinal TRPM7 to maintain their magnesium supply.
    primary_references
    [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    tissue
    Intestinal enterocytes; serum
    tissue_or_cell_type
    Intestinal enterocytes; serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 975–986

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Villin1-Cre conditional deletion and mineral phenotyping · source_derived_draft · unverified_draft

    ### intestinal-trpm7-loss-magnesium Intestinal Trpm7 deletion lowered magnesium availability in early postnatal mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Suckling mice required intestinal TRPM7 to maintain their magnesium supply. organism: Mouse tissue_or_cell_type: Intestinal enterocytes; serum experimental_model: Villin1-Cre conditional deletion and mineral phenotyping limitations: Early developmental model; not a test of dietary Mg restriction. evidence-system: Villin1-Cre conditional deletion and mineral phenotyping tissue: Intestinal enterocytes; serum [mittermeier-2019-trpm7] TRPM7 is the central gatekeeper of intestinal mineral absorption essential for postnatal survival (2019). https://pubmed.ncbi.nlm.nih.gov/30770447/ DOI: 10.1073/pnas.1810633116
    Complete structured claim and evidence

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

    Magnesium → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence-system
    Crossover feeding and biochemical monitoring
    experimental_model
    Crossover feeding and biochemical monitoring
    exposure
    Chemically measured mean intake: 130 mg Mg/day in the low period versus 411 mg/day in the supplemented period; 81 days per period after 10-day equilibration. These are experimental exposures, not recommendations.
    limitations
    A study-specific biomarker observation; not a diagnostic rule for all normal serum values.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    A normal-range serum result did not rule out the diet-related electrical phenotype in these participants.
    primary_references
    [klevay-2002-ectopy] Low dietary magnesium increases supraventricular ectopy (2002). https://ajcn.nutrition.org/article/S0002-9165%2823%2906154-3/fulltext DOI: 10.1093/ajcn/75.3.550
    tissue
    Serum, erythrocytes and urine
    tissue_or_cell_type
    Serum, erythrocytes and urine
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1332–1344

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Crossover feeding and biochemical monitoring · source_derived_draft · unverified_draft

    ### low-magnesium-diet-without-hypomagnesemia Mg biomarkers declined on the low-Mg diet, but hypomagnesemia, hypocalcemia and hypokalemia were not detected. Condition category: biomarker_context nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A normal-range serum result did not rule out the diet-related electrical phenotype in these participants. organism: Human tissue_or_cell_type: Serum, erythrocytes and urine experimental_model: Crossover feeding and biochemical monitoring limitations: A study-specific biomarker observation; not a diagnostic rule for all normal serum values. exposure: Chemically measured mean intake: 130 mg Mg/day in the low period versus 411 mg/day in the supplemented period; 81 days per period after 10-day equilibration. These are experimental exposures, not recommendations. evidence-system: Crossover feeding and biochemical monitoring tissue: Serum, erythrocytes and urine [klevay-2002-ectopy] Low dietary magnesium increases supraventricular ectopy (2002). https://ajcn.nutrition.org/article/S0002-9165%2823%2906154-3/fulltext DOI: 10.1093/ajcn/75.3.550
    Complete structured claim and evidence

  5. Kidney-restricted Trpm6 deletion did not lower serum Mg or raise urinary Mg in the tested mice.

    Kidney-specific Trpm6-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Ksp-Cre conditional deletion; six-month-old male mice
    experimental_model
    Ksp-Cre conditional deletion; six-month-old male mice
    limitations
    Bone Mg was slightly reduced; this is not proof renal TRPM6 is dispensable under every diet or in humans.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    These mice maintained circulating magnesium after kidney-specific TRPM6 loss.
    primary_references
    [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    tissue
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 936–947

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ksp-Cre conditional deletion; six-month-old male mice · source_derived_draft · unverified_draft

    ### renal-trpm6-loss-serum-preserved Kidney-restricted Trpm6 deletion did not lower serum Mg or raise urinary Mg in the tested mice. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: These mice maintained circulating magnesium after kidney-specific TRPM6 loss. organism: Mouse tissue_or_cell_type: Kidney; serum and urine experimental_model: Ksp-Cre conditional deletion; six-month-old male mice limitations: Bone Mg was slightly reduced; this is not proof renal TRPM6 is dispensable under every diet or in humans. evidence-system: Ksp-Cre conditional deletion; six-month-old male mice tissue: Kidney; serum and urine [chubanov-2016-trpm6] Epithelial magnesium transport by TRPM6 is essential for prenatal development and adult survival (2016). https://elifesciences.org/articles/20914 DOI: 10.7554/eLife.20914
    Complete structured claim and evidence

  6. Slc41a1-null mice maintained serum and urinary Mg similarly to littermates under standard and Mg-restricted diets.

    Slc41a1-null mouse genotype → Serum magnesium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Constitutive knockout with dietary Mg restriction challenge
    experimental_model
    Constitutive knockout with dietary Mg restriction challenge
    limitations
    Does not prove absence of all cell-specific functions; zebrafish and overexpression findings have different scope.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mouse
    plain_language
    Deleting SLC41A1 did not make these mice uniquely unable to maintain magnesium balance.
    primary_references
    [ilenwabor-2022-slc41a1] SLC41A1 knockout mice display normal magnesium homeostasis (2022). https://pubmed.ncbi.nlm.nih.gov/36049064/ DOI: 10.1152/ajprenal.00101.2022
    tissue
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1195–1206

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Constitutive knockout with dietary Mg restriction challenge · source_derived_draft · unverified_draft

    ### slc41a1-null-mouse-magnesium-preserved Slc41a1-null mice maintained serum and urinary Mg similarly to littermates under standard and Mg-restricted diets. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Deleting SLC41A1 did not make these mice uniquely unable to maintain magnesium balance. organism: Mouse tissue_or_cell_type: Kidney; serum and urine experimental_model: Constitutive knockout with dietary Mg restriction challenge limitations: Does not prove absence of all cell-specific functions; zebrafish and overexpression findings have different scope. evidence-system: Constitutive knockout with dietary Mg restriction challenge tissue: Kidney; serum and urine [ilenwabor-2022-slc41a1] SLC41A1 knockout mice display normal magnesium homeostasis (2022). https://pubmed.ncbi.nlm.nih.gov/36049064/ DOI: 10.1152/ajprenal.00101.2022
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CNNM2 variants in the reported families associated with hypomagnesemia, seizures and developmental impairment.

    Pathogenic CNNM2 variants → CNNM2-associated neurodevelopmental phenotype source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Five unrelated families plus functional and zebrafish evidence
    experimental_model
    Five unrelated families plus functional and zebrafish evidence
    limitations
    Neurological features persisted despite supplementation; do not equate the full genetic phenotype with reversible dietary Mg deficiency.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    This inherited disorder includes neurological abnormalities alongside low magnesium.
    primary_references
    [arjona-2014-cnnm2] CNNM2 Mutations Cause Impaired Brain Development and Seizures in Patients with Hypomagnesemia (2014). https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004267 DOI: 10.1371/journal.pgen.1004267
    tissue
    Kidney and nervous system
    tissue_or_cell_type
    Kidney and nervous system
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1125–1136

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five unrelated families plus functional and zebrafish evidence · source_derived_draft · unverified_draft

    ### cnnm2-variants-neurodevelopment CNNM2 variants in the reported families associated with hypomagnesemia, seizures and developmental impairment. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This inherited disorder includes neurological abnormalities alongside low magnesium. organism: Human tissue_or_cell_type: Kidney and nervous system experimental_model: Five unrelated families plus functional and zebrafish evidence limitations: Neurological features persisted despite supplementation; do not equate the full genetic phenotype with reversible dietary Mg deficiency. evidence-system: Five unrelated families plus functional and zebrafish evidence tissue: Kidney and nervous system [arjona-2014-cnnm2] CNNM2 Mutations Cause Impaired Brain Development and Seizures in Patients with Hypomagnesemia (2014). https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004267 DOI: 10.1371/journal.pgen.1004267
    Complete structured claim and evidence

  2. Two homozygous EGF P1070L sisters had low serum magnesium with inappropriately sustained urinary Mg loss.

    Pro-EGF P1070L → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-system
    Human pedigree and serum/urine phenotyping
    experimental_model
    Human pedigree and serum/urine phenotyping
    limitations
    Small kindred; cellular sorting experiments support the explanation rather than directly measuring the entire cascade in vivo.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Human
    plain_language
    The inherited EGF defect was linked to failure of the kidneys to conserve magnesium.
    primary_references
    [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
    tissue
    Kidney; serum and urine
    tissue_or_cell_type
    Kidney; serum and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1043–1054

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pedigree and serum/urine phenotyping · source_derived_draft · unverified_draft

    ### egf-variant-human-magnesium-wasting Two homozygous EGF P1070L sisters had low serum magnesium with inappropriately sustained urinary Mg loss. Condition category: machinery_impairment nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The inherited EGF defect was linked to failure of the kidneys to conserve magnesium. organism: Human tissue_or_cell_type: Kidney; serum and urine experimental_model: Human pedigree and serum/urine phenotyping limitations: Small kindred; cellular sorting experiments support the explanation rather than directly measuring the entire cascade in vivo. evidence-system: Human pedigree and serum/urine phenotyping tissue: Kidney; serum and urine [groenestege-2007-egf] Impaired basolateral sorting of pro-EGF causes isolated recessive renal hypomagnesemia (2007). https://www.jci.org/articles/view/31680 DOI: 10.1172/JCI31680
    Complete structured claim and evidence

  3. Two of three adults with homozygous PCBD1 mutations had hypomagnesemia with renal magnesium loss.

    Human pterin-4-alpha-carbinolamine dehydratase / PCBD1 → Urinary magnesium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Small human case series, three adults with homozygous PCBD1 mutations.
    limitations
    Two also had MODY-like diabetes regardless of magnesium status; neither finding establishes that phenylalanine supplements cause or correct the disorder.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    A genetic defect can connect abnormal phenylalanine handling with magnesium wasting.
    primary_references
    Mutations in PCBD1 cause hypomagnesemia and renal magnesium wasting. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24204001/ · DOI 10.1681/ASN.2013040337
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 94–100

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Small human case series, three adults with homozygous PCBD1 mutations. · source_derived_draft · unverified_draft

    ## l-phenylalanine-pcbd-magnesium A genetic defect can connect abnormal phenylalanine handling with magnesium wasting. Two of three adults with homozygous PCBD1 mutations had hypomagnesemia with renal magnesium loss. Model: Small human case series, three adults with homozygous PCBD1 mutations. Limitations: Two also had MODY-like diabetes regardless of magnesium status; neither finding establishes that phenylalanine supplements cause or correct the disorder. Evidence access: Primary abstract Mutations in PCBD1 cause hypomagnesemia and renal magnesium wasting. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24204001/ · DOI 10.1681/ASN.2013040337
    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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