Component

Biochemically low copper status

Biochemically low copper status. Species, exposure and limitations are retained in each linked claim.

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 it acts on

  1. In the sixteen-person longitudinal group, plasma copper and ceruloplasmin declined over follow-up, with a reported copper-deficiency incidence of 18.8%.

    Biochemically low copper status → Serum ceruloplasmin concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/21876546.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8", "start_char": 0, "end_char": 1842, "text_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8"}
    experimental_model
    Post-Roux-en-Y clinic cohort and longitudinal subset
    exposure
    136-person clinic cohort; separate longitudinal group of sixteen
    limitations
    Clinic selection and small longitudinal sample limit generalization; the study does not establish the sole molecular cause of every postoperative symptom.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human
    plain_language
    Following the same people over time detected falling copper-related measures.
    primary_references
    [copper-p21876546] Incidence and prevalence of copper deficiency following roux-en-y gastric bypass surgery. (2012). https://pubmed.ncbi.nlm.nih.gov/21876546/ DOI: 10.1038/ijo.2011.159
    tissue_or_cell_type
    Blood and clinical findings after gastric bypass
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1404–1415

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Post-Roux-en-Y clinic cohort and longitudinal subset · source_derived_draft · unverified_draft

    ### copper-bypass-cp-timecourse In the sixteen-person longitudinal group, plasma copper and ceruloplasmin declined over follow-up, with a reported copper-deficiency incidence of 18.8%. Condition category: nutrient_deficiency nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Following the same people over time detected falling copper-related measures. organism: Human tissue_or_cell_type: Blood and clinical findings after gastric bypass experimental_model: Post-Roux-en-Y clinic cohort and longitudinal subset limitations: Clinic selection and small longitudinal sample limit generalization; the study does not establish the sole molecular cause of every postoperative symptom. exposure: 136-person clinic cohort; separate longitudinal group of sixteen evidence_span: {"source_cache": "artifacts/copper-research/21876546.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8", "start_char": 0, "end_char": 1842, "text_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8"} [copper-p21876546] Incidence and prevalence of copper deficiency following roux-en-y gastric bypass surgery. (2012). https://pubmed.ncbi.nlm.nih.gov/21876546/ DOI: 10.1038/ijo.2011.159
    Complete structured claim and evidence

What acts on it

  1. Copper deficiency was identified in 13 of 136 clinic patients after Roux-en-Y gastric bypass; many had anemia, leukopenia or neuromuscular abnormalities.

    Roux-en-Y gastric bypass → Biochemically low copper status source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/21876546.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8", "start_char": 0, "end_char": 1842, "text_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8"}
    experimental_model
    Post-Roux-en-Y clinic cohort and longitudinal subset
    exposure
    136-person clinic cohort; separate longitudinal group of sixteen
    limitations
    The study observed postoperative deficiency; it did not directly quantify copper absorption in these participants. The 9.6% prevalence is specific to this clinic cohort.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human
    plain_language
    After this surgery, some patients developed a clinically important copper shortage.
    primary_references
    [copper-p21876546] Incidence and prevalence of copper deficiency following roux-en-y gastric bypass surgery. (2012). https://pubmed.ncbi.nlm.nih.gov/21876546/ DOI: 10.1038/ijo.2011.159
    tissue_or_cell_type
    Blood and clinical findings after gastric bypass
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1391–1402

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Post-Roux-en-Y clinic cohort and longitudinal subset · source_derived_draft · unverified_draft

    ### copper-bypass-lowcu Copper deficiency was identified in 13 of 136 clinic patients after Roux-en-Y gastric bypass; many had anemia, leukopenia or neuromuscular abnormalities. Condition category: nutrient_deficiency nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: After this surgery, some patients developed a clinically important copper shortage. organism: Human tissue_or_cell_type: Blood and clinical findings after gastric bypass experimental_model: Post-Roux-en-Y clinic cohort and longitudinal subset limitations: The study observed postoperative deficiency; it did not directly quantify copper absorption in these participants. The 9.6% prevalence is specific to this clinic cohort. exposure: 136-person clinic cohort; separate longitudinal group of sixteen evidence_span: {"source_cache": "artifacts/copper-research/21876546.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8", "start_char": 0, "end_char": 1842, "text_sha256": "29b1cc8c0170160c3a7b3449d807bbf309f6e1fa230e453fbfa467fe23fa71c8"} [copper-p21876546] Incidence and prevalence of copper deficiency following roux-en-y gastric bypass surgery. (2012). https://pubmed.ncbi.nlm.nih.gov/21876546/ DOI: 10.1038/ijo.2011.159
    Complete structured claim and evidence

  2. SCO2 overexpression suppressed the cellular copper-deficiency phenotype; SCO1 overexpression did not provide the same rescue.

    Human cytochrome c oxidase assembly protein SCO2 → Biochemically low copper status source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/17189203.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698", "start_char": 0, "end_char": 950, "text_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698"}
    experimental_model
    SCO1/SCO2 patient-cell analysis and genetic complementation
    exposure
    Pathogenic SCO variants; transporter and rescue assays
    limitations
    Copper effects varied with allele and tissue. A genetic assembly defect does not prove inadequate intake or universal response to copper supplementation.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Human
    plain_language
    Similar-looking proteins are not interchangeable repairs.
    primary_references
    [copper-p17189203] The human cytochrome c oxidase assembly factors SCO1 and SCO2 have regulatory roles in the maintenance of cellular copper homeostasis. (2007). https://pubmed.ncbi.nlm.nih.gov/17189203/ DOI: 10.1016/j.cmet.2006.12.001
    tissue_or_cell_type
    Patient-derived cellular systems
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 728–739

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SCO1/SCO2 patient-cell analysis and genetic complementation · source_derived_draft · unverified_draft

    ### copper-sco2-rescue-specificity SCO2 overexpression suppressed the cellular copper-deficiency phenotype; SCO1 overexpression did not provide the same rescue. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Similar-looking proteins are not interchangeable repairs. organism: Human tissue_or_cell_type: Patient-derived cellular systems experimental_model: SCO1/SCO2 patient-cell analysis and genetic complementation limitations: Copper effects varied with allele and tissue. A genetic assembly defect does not prove inadequate intake or universal response to copper supplementation. exposure: Pathogenic SCO variants; transporter and rescue assays evidence_span: {"source_cache": "artifacts/copper-research/17189203.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698", "start_char": 0, "end_char": 950, "text_sha256": "7653227df0fe557c484a72eafed6a7a96dc06f5d4f63f7eea4a5b9568949a698"} [copper-p17189203] The human cytochrome c oxidase assembly factors SCO1 and SCO2 have regulatory roles in the maintenance of cellular copper homeostasis. (2007). https://pubmed.ncbi.nlm.nih.gov/17189203/ DOI: 10.1016/j.cmet.2006.12.001
    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