Outcome
    Strong Evidence

    Vitamin E for Reduced Oxidative Stress

    High-dose vitamin E is the clearest example of antioxidant supplementation causing net harm.

    Overview

    High-dose vitamin E is the clearest example of antioxidant supplementation causing net harm.

    Verdict

    Not supported

    How It Works

    Lipid-soluble radical scavenger that also suppresses adaptive redox signalling at high doses.

    Dosing & Protocol

    Typical dose

    Recommended dose
    Not recommended above dietary intake
    Expected timeframe
    n/a

    Protocol

    form
    Alpha-tocopherol; dietary sources - nuts, seeds, vegetable oils - meet the 15 mg/day RDA without risk
    duration
    Prevention trials ran 3-10 years
    co factor
    Evidence indicates no clinical benefit despite consistent marker effects. Vitamin E lowers F2-isoprostanes and lipid peroxidation reliably, confirming it does what it is supposed to biochemically. The outcome trials are the problem: HOPE and HOPE-TOO found no cardiovascular benefit and increased heart failure, SELECT found 400 IU/day increased prostate cancer incidence by 17%, the Miller meta-analysis found increased all-cause mortality above 400 IU/day, and cancer and cognitive prevention trials were null. Reducing measured oxidative stress did not improve health, which is the central lesson of the antioxidant era.
    titration
    Not applicable. The tolerable upper intake level is 1,000 mg/day, but harms appeared at 400 IU/day
    starting dose
    Not recommended. Trials used 400-800 IU/day of alpha-tocopherol

    Evidence

    What the studies say

    The SELECT trial found increased prostate cancer risk, and meta-analyses associate high doses with increased all-cause mortality and haemorrhagic stroke.

    No studies are yet linked to both Vitamin E and Reduced Oxidative Stress.

    Safety

    Caveats

    Also increases bleeding risk with anticoagulants.

    Less likely to help if

    Everyone - the outcome trials were null or harmful.

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