Component

Hematocrit

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

2 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

Where it participates (unsigned role)

  1. Zinc-only treatment was followed by lower serum ferritin and hematocrit; with added iron, ferritin increased and hematocrit was unchanged. Hemoglobin did not change in either group.

    Zinc gluconate → Serum ferritin concentration source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Iron (coadministered_nutrient); Hematocrit (measured_endpoint); Blood hemoglobin concentration (unchanged_endpoint)
    evidence_location
    Indexed primary abstract.
    evidence_span
    {"source_cache": "artifacts/zinc-clinical-sources/yadrick1989.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "e2d70d43dded75edb026cac237f238d9e59399db6094098796e169f20e819443", "utf8_bytes": 969}
    experimental_model
    Ten-week zinc or zinc-plus-iron intervention in adult women
    exposure
    50 mg elemental zinc/day as gluconate, with or without 50 mg iron/day as ferrous sulfate monohydrate.
    limitations
    Reported comparisons are within-group pretreatment versus 10 weeks, not placebo-adjusted effects. ESOD is a functional biomarker, not a diagnosis of symptomatic copper deficiency.
    nutrient_topic
    Zinc research collection; topical membership is not evidence of a direct dietary effect. · Zinc
    organism
    Homo sapiens
    plain_language
    Iron-status markers responded differently depending on whether iron accompanied zinc.
    primary_references
    [zn-clin-yadrick1989] Iron, copper, and zinc status: response to supplementation with zinc or zinc and iron in adult females. (1989). https://pubmed.ncbi.nlm.nih.gov/2912000/ DOI: 10.1093/ajcn/49.1.145
    tissue_or_cell_type
    Blood and erythrocytes

    Zinc: transport, enzyme loading, deficiency and nutrient interactions (2026-09-17) · lines 1196–1209

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-week zinc or zinc-plus-iron intervention in adult women · source_derived_draft · unverified_draft

    ### zn-clin-iron-markers Zinc-only treatment was followed by lower serum ferritin and hematocrit; with added iron, ferritin increased and hematocrit was unchanged. Hemoglobin did not change in either group. Condition category: normal nutrient_topic: Zinc research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron-status markers responded differently depending on whether iron accompanied zinc. organism: Homo sapiens tissue_or_cell_type: Blood and erythrocytes experimental_model: Ten-week zinc or zinc-plus-iron intervention in adult women limitations: Reported comparisons are within-group pretreatment versus 10 weeks, not placebo-adjusted effects. ESOD is a functional biomarker, not a diagnosis of symptomatic copper deficiency. exposure: 50 mg elemental zinc/day as gluconate, with or without 50 mg iron/day as ferrous sulfate monohydrate. cross_nutrient: Iron (coadministered_nutrient); Hematocrit (measured_endpoint); Blood hemoglobin concentration (unchanged_endpoint) evidence_location: Indexed primary abstract. evidence_span: {"source_cache": "artifacts/zinc-clinical-sources/yadrick1989.abstract.txt", "locator": "Primary indexed abstract; complete local file", "file_sha256": "e2d70d43dded75edb026cac237f238d9e59399db6094098796e169f20e819443", "utf8_bytes": 969} [zn-clin-yadrick1989] Iron, copper, and zinc status: response to supplementation with zinc or zinc and iron in adult females. (1989). https://pubmed.ncbi.nlm.nih.gov/2912000/ DOI: 10.1093/ajcn/49.1.145
    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