Component

Erythrocyte mean cell volume

Independent substance, clinical endpoint or measured readout; study context is retained with each finding.

3 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 acts on it

  1. Copper administration increased erythrocyte size and leukocyte counts in the reported index patient; the authors also reported correction of hypoceruloplasminemia in additional zinc-treated patients.

    Copper → Erythrocyte mean cell volume source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Zinc (prior_exposure); Blood leukocyte count (increased_endpoint); Serum ceruloplasmin concentration (responsive_marker)
    evidence_location
    Indexed primary abstract.
    evidence_span
    {"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487}
    experimental_model
    Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy
    exposure
    Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered.
    limitations
    Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    Copper replacement improved the reported blood-cell abnormalities.
    primary_references
    [zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019
    tissue_or_cell_type
    Blood copper and hematology
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1422–1435

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy · source_derived_draft · unverified_draft

    ### zn-clin-copper-response Copper administration increased erythrocyte size and leukocyte counts in the reported index patient; the authors also reported correction of hypoceruloplasminemia in additional zinc-treated patients. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper replacement improved the reported blood-cell abnormalities. organism: Homo sapiens tissue_or_cell_type: Blood copper and hematology experimental_model: Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy limitations: Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio. exposure: Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered. cross_nutrient: Zinc (prior_exposure); Blood leukocyte count (increased_endpoint); Serum ceruloplasmin concentration (responsive_marker) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487} [zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. An adult with sickle cell anemia developed hypocupremia after two years of zinc therapy, accompanied by microcytosis and relative neutropenia. Additional zinc-treated patients had varying hypoceruloplasminemia.

    Zinc → Plasma copper concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Copper (deficient_nutrient); Erythrocyte mean cell volume (reduced_endpoint); Blood neutrophil count (reduced_endpoint); Serum ceruloplasmin concentration (associated_marker)
    evidence_location
    Indexed primary abstract.
    evidence_span
    {"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487}
    experimental_model
    Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy
    exposure
    Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered.
    limitations
    Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    Long zinc treatment was associated with copper shortage and blood-cell changes.
    primary_references
    [zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019
    tissue_or_cell_type
    Blood copper and hematology
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1407–1420

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy · source_derived_draft · unverified_draft

    ### zn-clin-hypocupremia An adult with sickle cell anemia developed hypocupremia after two years of zinc therapy, accompanied by microcytosis and relative neutropenia. Additional zinc-treated patients had varying hypoceruloplasminemia. Condition category: nutrient_deficiency nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Long zinc treatment was associated with copper shortage and blood-cell changes. organism: Homo sapiens tissue_or_cell_type: Blood copper and hematology experimental_model: Clinical case and additional observations in adults with sickle cell anemia receiving zinc therapy limitations: Case evidence in a particular disease setting; dose and formulation are not verified from the abstract. Does not establish incidence or a universal zinc:copper supplement ratio. exposure: Index patient received zinc as an antisickling intervention for two years; copper was subsequently administered. cross_nutrient: Copper (deficient_nutrient); Erythrocyte mean cell volume (reduced_endpoint); Blood neutrophil count (reduced_endpoint); Serum ceruloplasmin concentration (associated_marker) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/prasad1978.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "7c4b85a9dd24c3e3bfd04414c0add5d0fa2bcc8c15b5e46bded351e2a2f01e3f", "utf8_bytes": 487} [zn-clin-prasad1978] Hypocupremia induced by zinc therapy in adults. (1978). https://pubmed.ncbi.nlm.nih.gov/359844/ DOI: 10.1001/jama.1978.03290200044019
    Complete structured claim and evidence

  2. Of 141 neurologic B12-deficiency patients, 34 had normal hematocrit, 25 normal mean cell volume, and 19 both; 40 lacked at least one of these two abnormalities.

    Vitamin B12 (cobalamins) → B12-associated neuropsychiatric impairment source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Clinical series: 141 consecutive patients with neuropsychiatric abnormalities attributed to cobalamin deficiency; 40 lacked anemia or macrocytosis.
    exposure
    Clinical evaluation and cobalamin replacement; observational response series.
    limitations
    The reported 28% is not the percentage with both tests normal. Selected patients do not estimate population prevalence.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Homo sapiens
    plain_language
    Normal red-cell size or hematocrit did not exclude the neurologic presentation.
    primary_references
    [b12-lindenbaum1988] Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis (1988). https://pubmed.ncbi.nlm.nih.gov/3374544/ DOI: 10.1056/nejm198806303182604
    tissue_or_cell_type
    Human blood or whole-person endpoints
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1426–1436

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clinical series: 141 consecutive patients with neuropsychiatric abnormalities attributed to cobalamin deficiency; 40 lacked anemia or macrocytosis. · source_derived_draft · unverified_draft

    ### b12-neuro-normal-blood-counts Of 141 neurologic B12-deficiency patients, 34 had normal hematocrit, 25 normal mean cell volume, and 19 both; 40 lacked at least one of these two abnormalities. Condition category: nutrient_deficiency nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Normal red-cell size or hematocrit did not exclude the neurologic presentation. organism: Homo sapiens tissue_or_cell_type: Human blood or whole-person endpoints experimental_model: Clinical series: 141 consecutive patients with neuropsychiatric abnormalities attributed to cobalamin deficiency; 40 lacked anemia or macrocytosis. limitations: The reported 28% is not the percentage with both tests normal. Selected patients do not estimate population prevalence. exposure: Clinical evaluation and cobalamin replacement; observational response series. [b12-lindenbaum1988] Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis (1988). https://pubmed.ncbi.nlm.nih.gov/3374544/ DOI: 10.1056/nejm198806303182604
    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.

    Evidence, AI assistance and curation standards