Component

Prostate cancer incidence

Prostate cancer incidence. Read linked claims for the population, experiment and limits.

4 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. The ATBC secondary analysis found 32% lower prostate-cancer incidence among men assigned alpha-tocopherol versus those not assigned it.

    Alpha-tocopherol → Prostate cancer incidence source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    ATBC randomized factorial trial secondary prostate-cancer endpoint; 29133 Finnish male smokers aged 50–69
    exposure
    Alpha-tocopherol 50 mg/day with or without beta-carotene 20 mg/day; median 6.1 years.
    limitations
    Secondary cancer endpoint in male smokers; differs from SELECT in dose, population and ascertainment. An opposite trial result is not automatically a same-condition biological contradiction. This result and SELECT must retain their different populations and regimens; neither supplies the molecular explanation for their difference.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    A lower-dose trial in male smokers found fewer prostate-cancer diagnoses.
    primary_references
    [e-clin-atbc1998] Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial. (1998). https://pubmed.ncbi.nlm.nih.gov/9521168/ DOI: 10.1093/jnci/90.6.440
    tissue_or_cell_type
    Prostate and whole-person outcomes

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1323–1334

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · ATBC randomized factorial trial secondary prostate-cancer endpoint; 29133 Finnish male smokers aged 50–69 · source_derived_draft · unverified_draft

    ### e-clin-atbc-prostate-incidence The ATBC secondary analysis found 32% lower prostate-cancer incidence among men assigned alpha-tocopherol versus those not assigned it. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: A lower-dose trial in male smokers found fewer prostate-cancer diagnoses. organism: Homo sapiens tissue_or_cell_type: Prostate and whole-person outcomes experimental_model: ATBC randomized factorial trial secondary prostate-cancer endpoint; 29133 Finnish male smokers aged 50–69 limitations: Secondary cancer endpoint in male smokers; differs from SELECT in dose, population and ascertainment. An opposite trial result is not automatically a same-condition biological contradiction. This result and SELECT must retain their different populations and regimens; neither supplies the molecular explanation for their difference. exposure: Alpha-tocopherol 50 mg/day with or without beta-carotene 20 mg/day; median 6.1 years. cross_nutrient: true [e-clin-atbc1998] Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial. (1998). https://pubmed.ncbi.nlm.nih.gov/9521168/ DOI: 10.1093/jnci/90.6.440
    Complete structured claim and evidence

  2. In the SELECT secondary analysis, vitamin E alone increased total prostate-cancer risk by 63% among men below the 40th percentile of baseline toenail selenium; a significant effect was not found above that split.

    All-rac-alpha-tocopheryl acetate → Prostate cancer incidence source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Secondary case-cohort analysis nested within SELECT; 1739 total cases and 3117 sampled cohort members
    exposure
    Trial supplementation analyzed by baseline toenail selenium; E-alone comparison used below versus at/above the 40th percentile.
    limitations
    Exploratory subgroup thresholds are cohort percentiles, not deficiency thresholds; baseline selenium was not randomized. Does not justify adding selenium to make high-dose vitamin E safe.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Baseline selenium measurements helped identify different trial outcomes, but did not establish a safe supplement combination.
    primary_references
    [e-clin-select2014] Baseline selenium status and effects of selenium and vitamin e supplementation on prostate cancer risk. (2014). https://pubmed.ncbi.nlm.nih.gov/24563519/ DOI: 10.1093/jnci/djt456
    tissue_or_cell_type
    Prostate and toenail selenium biomarker
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1310–1321

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Secondary case-cohort analysis nested within SELECT; 1739 total cases and 3117 sampled cohort members · source_derived_draft · unverified_draft

    ### e-clin-select-baseline-selenium In the SELECT secondary analysis, vitamin E alone increased total prostate-cancer risk by 63% among men below the 40th percentile of baseline toenail selenium; a significant effect was not found above that split. Condition category: biomarker_context nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Baseline selenium measurements helped identify different trial outcomes, but did not establish a safe supplement combination. organism: Homo sapiens tissue_or_cell_type: Prostate and toenail selenium biomarker experimental_model: Secondary case-cohort analysis nested within SELECT; 1739 total cases and 3117 sampled cohort members limitations: Exploratory subgroup thresholds are cohort percentiles, not deficiency thresholds; baseline selenium was not randomized. Does not justify adding selenium to make high-dose vitamin E safe. exposure: Trial supplementation analyzed by baseline toenail selenium; E-alone comparison used below versus at/above the 40th percentile. cross_nutrient: true [e-clin-select2014] Baseline selenium status and effects of selenium and vitamin e supplementation on prostate cancer risk. (2014). https://pubmed.ncbi.nlm.nih.gov/24563519/ DOI: 10.1093/jnci/djt456
    Complete structured claim and evidence

  3. SELECT did not demonstrate prostate-cancer prevention with vitamin E plus selenium (HR 1.05, 99% CI 0.89–1.22 versus placebo).

    All-rac-alpha-tocopheryl acetate → Prostate cancer incidence source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized
    exposure
    All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011.
    limitations
    Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism. The nonsignificant combination estimate is not proof that selenium mechanistically neutralizes vitamin E-associated harm.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Adding selenium did not demonstrate a prostate-cancer prevention benefit.
    primary_references
    [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    tissue_or_cell_type
    Prostate and whole-person outcomes

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1297–1308

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized · source_derived_draft · unverified_draft

    ### e-clin-select-combination-boundary SELECT did not demonstrate prostate-cancer prevention with vitamin E plus selenium (HR 1.05, 99% CI 0.89–1.22 versus placebo). Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding selenium did not demonstrate a prostate-cancer prevention benefit. organism: Homo sapiens tissue_or_cell_type: Prostate and whole-person outcomes experimental_model: SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized limitations: Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism. The nonsignificant combination estimate is not proof that selenium mechanistically neutralizes vitamin E-associated harm. exposure: All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011. cross_nutrient: true [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    Complete structured claim and evidence

  4. In SELECT, vitamin E alone increased prostate-cancer incidence relative to placebo (HR 1.17, 99% CI 1.004–1.36); the absolute increase was 1.6 cases per 1000 person-years.

    All-rac-alpha-tocopheryl acetate → Prostate cancer incidence source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized
    exposure
    All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011.
    limitations
    Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    The tested high-dose vitamin E preparation increased prostate-cancer diagnoses in this trial.
    primary_references
    [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    tissue_or_cell_type
    Prostate and whole-person outcomes

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1284–1295

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized · source_derived_draft · unverified_draft

    ### e-clin-select-prostate-incidence In SELECT, vitamin E alone increased prostate-cancer incidence relative to placebo (HR 1.17, 99% CI 1.004–1.36); the absolute increase was 1.6 cases per 1000 person-years. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The tested high-dose vitamin E preparation increased prostate-cancer diagnoses in this trial. organism: Homo sapiens tissue_or_cell_type: Prostate and whole-person outcomes experimental_model: SELECT randomized factorial prevention trial; 34887 men in primary analysis, 35533 originally randomized limitations: Trial-specific formulation, dose and population; does not establish the effect of food intake or of every vitamin E form. Group results cannot identify an intracellular mechanism. exposure: All-rac-alpha-tocopheryl acetate 400 IU/day; selenium arm 200 micrograms/day selenium as L-selenomethionine; supplements stopped in 2008, follow-up continued to July 2011. cross_nutrient: true [e-clin-select2011] Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). (2011). https://pubmed.ncbi.nlm.nih.gov/21990298/ DOI: 10.1001/jama.2011.1437
    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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