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This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.

Compact view
Research pass: thorough Compound SKIP-FOR-NOW HIGH

Vitamin E

Extended Research
High-risk compound

Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.

◈ Extended Research ◈

Our depth — beyond the mirror

Deeper analysis, verdict reasoning, and per-archetype recommendations from our research team.

▸ Editor's verdict SKIP-FOR-NOW HIGH

"Supplementation in non-deficient adults has failed every major prevention trial (HOPE, GISSI, Women's Health Study, Physicians' Health Study II, SELECT) and the Miller 2005 meta-analysis (PMID 15537682) flagged a dose-dependent all-cause mortality signal at ≥400 IU/day all-rac-α-tocopherol. ATBC + CARET + SELECT raised cancer concerns specifically. The user is a 20yo MMA athlete eating an animal-protein-rich diet (likely already replete in α-tocopherol from olive oil, almonds, spinach, sunflower seeds, fish oil). V4 fish oil softgels already contain mixed tocopherols as antioxidant preservatives. Genuine clinical-grade vitamin E indications are (a) severe deficiency syndromes (AVED, abetalipoproteinemia, fat malabsorption) — not relevant; (b) biopsy-proven non-diabetic NASH per PIVENS — not relevant absent NAFLD diagnosis. Mixed-tocotrienol products (especially annatto-derived γ-/δ-tocotrienol) sit on the WATCH-LIST: distinct mechanism from tocopherols (HMG-CoA reductase, NF-κB, ceramide), small RCT signals in NAFLD and lipids, but underpowered evidence and α-tocopherol displacement concerns. Verdict moves to OPTIONAL-ADD only if (1) genetic AVED is identified, (2) NAFLD is diagnosed on imaging/biopsy, or (3) a clean modern RCT of mixed tocotrienols establishes specific benefit for the user's training/longevity goals."

Research pass: thorough
▸ Decision matrix by user profile Per-archetype
  • 20-30, training-priority, animal-protein-rich diet (this-archetype)
    SKIP-FOR-NOW

    Food source covers RDA functionally. V4 fish oil already includes mixed tocopherol preservatives. No supplementation indication absent NASH or AVED diagnosis. Adding pill-based vitamin E without indication wastes both budget and the post-training antioxidant-adaptation balance (Ristow PNAS 2009 concern). WATCH-LIST mixed-tocotrienol product specifically — promising mechanism, underpowered evidence, revisit if a clean modern RCT establishes specific benefit.

  • 30-50, executive maintenance, mixed diet
    NEUTRAL

    / food source preferred. Same logic; no supplementation indication absent NASH diagnosis. If supplementing, mixed tocopherols 200-400 IU/day < α-tocopherol mega-dose.

  • 50+, longevity-focused
    SKIP-FOR-NOW

    Failed prevention-trial evidence applies most strongly to this group. Food source preferred. Possible exception: NASH diagnosis on imaging, then OPTIONAL-ADD per PIVENS 800 IU/day.

  • Diagnosed NASH, non-diabetic, biopsy-proven
    OPTIONAL-ADD

    per PIVENS protocol. RRR-α-tocopherol 800 IU/day, hepatology-supervised, INR monitoring. Single robust supplementation indication.

  • AVED / abetalipoproteinemia / severe fat malabsorption
    REQUIRED

    Lifelong α-tocopherol replacement is standard of care.

  • On warfarin / DOAC / antiplatelet
    AVOID

    supplementation. Bleeding risk amplified; food source only.

  • Active prostate cancer or strong family history
    AVOID

    supplementation. SELECT trial signal flagged 17% increased prostate cancer incidence at 400 IU/day.

  • Smoker / former smoker
    AVOID

    high-dose β-carotene + vitamin E combinations. ATBC + CARET concerns.

  • Endurance athlete optimizing training adaptation
    AVOID

    high-dose E + C around training. Ristow PNAS 2009 antioxidant-blunting of mitochondrial biogenesis and insulin-sensitivity adaptation.

▸ Subjective experience (deep)

Acute (single 200-1000 IU dose with fat-containing meal):

  • No subjective effects. Vitamin E does not produce noticeable acute changes in mood, cognition, energy, or sleep at any dose. This is a slow-acting structural antioxidant, not a CNS-active compound.
  • Fat-coadministration matters for absorption but does not produce subjective signal.
  • Some users report mild GI discomfort (bloating, loose stool) at 1000+ IU/day single doses.

Chronic (daily 200-800 IU/day for months):

  • No subjective signal at RDA-to-moderate doses in non-deficient adults.
  • At high doses (≥400 IU/day chronic), some users report mild bruising, longer bleeding from cuts, or bleeding gums — clinically significant in patients on anticoagulants or with bleeding diatheses. Stop signal.
  • AVED patients on replacement therapy report slow improvement in ataxia and neuropathy over months — but this is correction of frank deficiency, not supplementation effect.
  • NASH patients on PIVENS-style 800 IU/day: ALT/AST trend down within months; histologic improvement not assessable subjectively, requires biopsy.

Honest summary: Vitamin E does not feel like anything. The idea that you "feel" antioxidants is largely placebo-driven; the genuine value is in slow structural maintenance (membrane integrity, lipid integrity in stored fish oil, etc.) and in correcting frank deficiency. For users in this archetype, expect zero subjective signal whether or not the supplement is taken — which is itself a reason to weight evidence-based clinical indications heavily over felt-effect heuristics.

▸ Tolerance + cycling deep dive
  • Tolerance buildup: None — vitamin E is not a receptor-mediated compound; no pharmacodynamic tolerance.
  • Tissue saturation: at chronic supplementation, plasma and adipose α-tocopherol reach steady state; further intake increases excretion of γ-tocopherol metabolites and CEHCs.
  • Cycling: not needed at RDA dose; food-source intake is naturally cycled by diet variation.
  • Discontinuation: plasma α-tocopherol falls slowly over weeks-months due to adipose stores; no withdrawal effect.
▸ Stacking deep dive

Synergistic with

  • Vitamin C (ascorbate) — recycles α-tocopheroxyl radical at the aqueous-lipid membrane interface; the foundational pairing. Consensus dosing: vitamin C 200-500 mg/day from food + supplement; vitamin E from food. Avoid high-dose pill-based both around training (Ristow PNAS 2009 antioxidant-blunting concern).
  • Glutathione (GSH) / NAC — GSH regenerates dehydroascorbate to ascorbate, completing the redox triad. NAC supports GSH synthesis. The full E → C → GSH network is the integrated membrane antioxidant system.
  • Selenium — cofactor for GPx4, which clears lipid hydroperoxides downstream of vitamin E's chain-breaking step. Adequate selenium status (~55-100 mcg/day, food-source: Brazil nuts, fish, eggs) supports vitamin E function. Avoid high-dose Se + E combination (SELECT trial showed no benefit and active harm signal in vitamin E arm).
  • Astaxanthin — both lipid-soluble membrane antioxidants; complementary positioning (astaxanthin spans the bilayer, α-tocopherol localizes near the aqueous interface). Often co-recommended in skin/eye/UV protection protocols.
  • Fish oil (omega-3 / DHA) — PUFA-rich fish oil is highly susceptible to lipid peroxidation; vitamin E protects omega-3s from oxidation in the membrane and during storage. Most fish oil products (including the user's V4 Carlson Super DHA Gems) include mixed tocopherols as antioxidant preservatives in the formulation itself — this often provides meaningful daily vitamin E intake without separate supplementation.
  • Coenzyme Q10 / ubiquinol — CoQ10 is a separate mitochondrial-membrane antioxidant; mechanism-aligned, no direct interaction. Acceptable co-administration.

Avoid stacking with

  • Anticoagulants (warfarin, rivaroxaban, apixaban, dabigatran) — high-dose vitamin E antagonizes vitamin K-dependent clotting factors and inhibits platelet aggregation. Monitor INR closely or avoid.
  • Antiplatelets (aspirin, clopidogrel, prasugrel) — additive bleeding risk at high vitamin E doses.
  • High-dose synthetic α-tocopherol (>400 IU/day) in non-deficient adults — Miller 2005 mortality signal.
  • High-dose β-carotene (>15-20 mg/day) in current/former smokers — CARET/ATBC concerns about carotenoid + smoking interaction; some carotenoid-vitamin E products bundle these; avoid.
  • Statins + niacin (HATS context) — high-dose vitamin E may attenuate HDL response to statin/niacin combination; relevance at RDA unclear.
  • α-tocopherol + tocotrienol same-time dosing — α-TTP displacement reduces tocotrienol uptake. Separate by 8-12 hours if both used.

Neutral / safe co-administration

  • All V4 OTC stack items (DHA, magnesium, citicoline, NAC, phosphatidylserine, curcumin, rhodiola, theanine, glycine/tryptophan, D3+K2, beta-alanine, vitamin C, creatine) — no flagged interactions; some synergistic (vitamin C, NAC, fish oil).
  • BPC-157, TB-500 (peptides) — different mechanisms.
  • Modafinil, bromantane, racetams — no flagged interactions.
  • Astaxanthin, apigenin, idebenone — antioxidant-class neutral-to-synergistic.
▸ Drug interactions deep dive
  • Warfarin / DOACs / antiplatelets — high-dose vitamin E increases bleeding risk via vitamin K antagonism + platelet inhibition. Monitor INR; avoid >100 IU/day if possible.
  • Statins — possible attenuation of HDL response (HATS); clinical relevance at RDA unclear.
  • Cyclosporine — vitamin E TPGS form (water-soluble) increases cyclosporine bioavailability significantly; standard tocopherol forms do not. Specialist context.
  • Chemotherapy — antioxidant supplementation during chemotherapy is controversial; some evidence high-dose vitamin E may reduce efficacy of pro-oxidant agents (anthracyclines, platinums). Avoid during active chemo without oncologist guidance.
  • CYP3A4 substrates — α-tocopherol modestly induces CYP3A4 at high doses; clinical relevance generally low.
  • Iron supplements — vitamin E may modestly reduce iron absorption when co-dosed; separate by 2 hours if both required.
  • Bile acid sequestrants (cholestyramine, colestipol) — reduce vitamin E absorption; increase intake or separate dosing.
  • Orlistat — reduces fat absorption including vitamin E; supplementation may be needed in chronic users.
▸ Pharmacogenomics
  • α-TTP (TTPA gene) variants — homozygous loss-of-function causes AVED. Heterozygous variants generally subclinical but may produce mildly reduced plasma α-tocopherol; clinically usually not significant.
  • APOE variants — α-tocopherol is transported on lipoproteins; APOE4 carriers have altered lipoprotein metabolism and may have different vitamin E pharmacokinetics. Some preclinical and observational data suggest APOE4 carriers may benefit less (or be harmed more) by high-dose vitamin E supplementation. Worth noting for the user's pending 23andMe APOE results (~June 5-15, 2026).
  • CYP4F2 V433M (rs2108622) — V433M variant (~30% frequency) reduces ω-hydroxylation of α-tocopherol, leading to higher plasma α-tocopherol at given intake. This may also affect warfarin metabolism (CYP4F2 metabolizes vitamin K1) — variant carriers need higher warfarin doses. If user has this variant + ever needs anticoagulation, vitamin E interaction concerns are amplified.
  • CYP3A4 variants — minor effect on α-tocopherol clearance.
  • GPx4 variants — affect downstream lipid hydroperoxide clearance; theoretical relevance to vitamin E function but no actionable clinical data.
  • Practical: check 23andMe results when available. APOE genotype is the most relevant pharmacogenomic flag for the user's vitamin E decisions.
▸ Sourcing deep dive
Path Vendor Cost Reliability Notes
Food source Sunflower seeds, almonds, spinach, olive oil, fish oil $0 incremental Highest Recommended for the user. Diet variety provides 15-30 mg/day α-tocopherol naturally.
OTC mixed tocopherols Pure Encapsulations Vitamin E (mixed tocopherols 400 IU) ~$15-20 / 90 ct High Preferred form if supplementing; preserves γ-tocopherol. Third-party tested.
OTC mixed tocopherols Thorne Ultimate-E (mixed tocopherols + tocotrienols 67 mg) ~$20-25 / 60 ct High Mixed family product; tocopherol + tocotrienol blend.
OTC d-alpha-tocopherol NOW Foods d-Alpha Tocopheryl 400 IU ~$10-15 / 250 ct High Natural form; cheapest reasonable option.
OTC tocotrienols (annatto) A.C. Grace Unique E Tocotrienol or DeltaGold formulations ~$30-50 / 60-90 ct Medium-high If pursuing tocotrienol-specific protocol. Annatto-source preferred (no α-tocopherol contamination).
OTC tocotrienols (palm) Carotech EVNol / palm tocotrienol products ~$20-30 Medium Palm-derived; contains some α-tocopherol contamination. Less ideal than annatto.
Avoid High-dose synthetic dl-α-tocopherol (>400 IU) — — Miller 2005 + SELECT signals; not recommended in non-deficient adults.
Avoid Bargain "Vitamin E" supplements with no form specification — — Likely synthetic dl-form; lower bioactivity, mortality-trial dose territory if 400+ IU.
Rx Vedolimab (vitamin E TPGS for cystic fibrosis / AVED) Variable Specialist Only relevant for specific deficiency syndromes.

Sourcing notes:

  1. For users in this archetype: food source covers it. Almonds + olive oil + V4 fish oil softgels' built-in tocopherol preservatives provide 15-30 mg/day α-tocopherol functionally — at or above RDA, without any pill.
  2. If supplementing despite consensus: mixed tocopherols (Pure Encapsulations or Thorne) at 200-400 IU/day stays well below the Miller 2005 threshold and preserves γ-tocopherol.
  3. Tocotrienol-specific protocols: annatto-derived (DeltaGold-spec) is the cleanest sourcing; avoid palm-derived products with α-tocopherol contamination if using tocotrienols specifically. Dose 8-12 hours separated from any α-tocopherol-containing supplement.
  4. Cost is essentially trivial across all paths — even premium mixed-tocopherol supplements run <$25/month.
  5. Quality flags: demand RRR-α-tocopherol or "d-alpha-tocopherol" labeling; reject "dl-alpha-tocopherol" or "all-rac" without justification. For tocotrienols, demand annatto or specific isoform breakdown on the COA.
▸ Biomarkers to track (deep)

Baseline (only if supplementing or evaluating deficiency)

  • Serum α-tocopherol (normal: 5-20 mg/L; deficiency: <5 mg/L). Best assessed as **vitamin E:total lipid ratio** (>0.8 mg/g indicates adequate; <0.6 mg/g indicates deficiency) to correct for hyperlipidemia confound.
  • Lipid panel (total cholesterol, LDL, HDL, triglycerides) — needed to interpret vitamin E:lipid ratio.
  • ALT / AST — baseline for NASH context.
  • GGT — supplementary NAFLD marker.
  • CBC + INR — baseline before any high-dose supplementation, especially if any anticoagulant interaction risk.

During use

  • NASH protocol: ALT/AST every 3 months; periodic GGT; annual lipid panel; INR if any anticoagulant risk; vitamin E level annually.
  • High-dose supplementation (any indication): INR every 3 months; CBC if bruising/bleeding concerns.
  • Subjective: any unusual bruising, bleeding gums, prolonged bleeding from cuts, headache. STOP signal.

Post-cycle

  • Plasma α-tocopherol falls slowly (weeks-months) due to adipose stores; no rebound effect.
▸ Controversies / open debates Live debate

  • Why did every prevention trial fail? Multiple competing hypotheses:

    1. Healthy-cohort floor effect — RCT subjects were already vitamin-E-replete from food, so supplementation provided no additional benefit. Strong empirical case: trials in deficient populations (AVED, NASH) succeeded.
    2. Wrong isoform — α-tocopherol-only supplementation displaced γ-tocopherol, blunting reactive nitrogen species defense. Mixed-tocopherol formulations might have done better but were not used.
    3. Wrong dose — high-dose mega-supplementation (400-2000 IU/day) is mechanistically distinct from physiologic intake (15-30 mg/day) and may produce paradoxical pro-oxidant effects via redox-cycle imbalance with vitamin C / GSH.
    4. Wrong endpoint — chain-breaking lipid antioxidant effect may matter for chronic neurodegeneration (slow-onset) but not for acute vascular events (CV trial endpoints).
    5. Synthetic vs natural — most CV trials used dl-α-tocopherol (synthetic 8-stereoisomer mix); only RRR-α is α-TTP-retained efficiently. Bioactivity ratio may have been overestimated.
    6. Genuine null — vitamin E supplementation simply does not reduce CV events or cancer in non-deficient adults, regardless of form or dose. Most likely explanation given the breadth of failures.

  • The Miller 2005 controversy. Some authors challenged the meta-analysis methodology (heterogeneity in trial populations, dose-response modeling assumptions). Berry et al. and others published competing meta-analyses with smaller or no mortality signal at narrower dose ranges. Consensus view in 2026: the high-dose mortality signal is real, even if magnitude is debated. AHA, AND, and clinical guidelines recommend against high-dose vitamin E supplementation for prevention.

  • SELECT prostate cancer mechanism. No clear mechanism for the 17% increased prostate cancer incidence in α-tocopherol arm. Hypotheses: γ-tocopherol displacement (γ-tocopherol may be the protective form in prostate); selegylation of chromanol structure mimicking estrogenic activity; chance finding given multiple endpoints. Mechanistic uncertainty makes the signal hard to dismiss as artifact.

  • NASH efficacy reproducibility. PIVENS is a single major RCT. Some smaller trials replicate; pediatric TONIC was mixed. AASLD recommendation rests primarily on PIVENS. Field is awaiting larger replication and longer-term safety data.

  • Tocotrienol enthusiasm vs evidence. Tocotrienol research has grown rapidly post-2010 with promising mechanism work and small RCT signals (NAFLD, lipids, bone). The biohacker community has run ahead of the evidence base. For users in this archetype WATCH-LIST is appropriate: mechanism is real and distinct, RCTs are underpowered, displacement issues with α-tocopherol are unresolved. Wait for a clean modern trial before promoting from WATCH-LIST.

  • Mixed tocopherol vs synthetic α-tocopherol — does it actually matter? Mechanistically yes (γ-tocopherol preservation), but no major RCT has compared mixed-tocopherol vs α-tocopherol-only supplementation head-to-head with hard endpoints. Most clinical evidence is on α-tocopherol monotherapy because that's what trials used. Practical advice: mixed tocopherols are mechanism-superior; clinical-outcome evidence is limited.

  • Antioxidant-blunting of training adaptation (Ristow 2009 PNAS). Vitamin E + C 1000 mg/day blunted mitochondrial biogenesis and insulin sensitivity adaptation in trained men. Replicated in some but not all subsequent studies. For an MMA athlete optimizing training adaptation, even modest pill-based E + C around training is mechanistically counterproductive. Food-source vitamin E during training window is fine.

  • Subclinical deficiency in athletes vs sedentary. Some preclinical work suggests athletes have higher vitamin E turnover due to PUFA oxidation during training. Clinical relevance: no robust RCT in athletes shows supplementation benefit beyond food source. Probably not a meaningful concern with adequate diet.

▸ Verdict change log
  • 2026-05-10 — Initial verdict: SKIP-FOR-NOW supplementation in non-deficient adults; WATCH-LIST mixed-tocotrienol product specifically. Verdict-confidence HIGH for the SKIP-FOR-NOW position given (a) Miller 2005 dose-dependent mortality signal at ≥400 IU/day, (b) failed CV prevention RCTs (HOPE, GISSI, Women's Health Study, Physicians' Health Study II), (c) ATBC + CARET + SELECT cancer signals, (d) consensus shift to food-source preference, (e) genuine clinical indications (AVED, NASH) not relevant to user. WATCH-LIST mixed-tocotrienol position because (a) mechanism distinct from tocopherols (HMG-CoA reductase, NF-κB, ceramide), (b) small RCTs show signal in NAFLD and lipids, (c) α-tocopherol displacement / contamination issues unresolved in current products, (d) underpowered evidence base. Verdict moves to OPTIONAL-ADD if (1) NAFLD diagnosed on imaging/biopsy → PIVENS protocol RRR-α-tocopherol 800 IU/day, (2) AVED-spectrum genetic deficiency identified (very unlikely given pending 23andMe), or (3) a clean modern (post-2024) tocotrienol RCT establishes specific benefit for the user's training/longevity goals.
▸ Open questions / gaps Open
  • Will any large modern RCT specifically test mixed-tocopherol vs isolated α-tocopherol vs placebo with hard endpoints? Unlikely commercial sponsor given off-patent status; only NIH-style funding could mount this. Mechanism case is strong; outcome data is the missing piece.
  • Are annatto-derived tocotrienols clinically distinct from palm-derived in human RCTs? Mostly in vitro / preclinical evidence; few head-to-head human trials. Worth tracking through 2026-2028.
  • Does APOE4 genotype interact with vitamin E supplementation outcomes? Some observational hint but no prospective RCT subgroup analysis. User's pending 23andMe APOE results may add personal relevance.
  • Long-term safety of PIVENS-style 800 IU/day NASH protocol beyond 96 weeks? PIVENS extension data exists but is limited. AASLD recommendation assumes ongoing benefit at chronic dosing; long-term cancer/CV safety is the open question.
  • Is the Ristow 2009 antioxidant-blunting effect dose-dependent and form-dependent? Mostly tested with high-dose isolated synthetic forms; food-source data on training adaptation is sparse.
  • Why does α-tocopherol seem to interact with selenium so unfavorably in SELECT but synergistically in livestock studies? Mechanistic puzzle; possibly different baseline selenium status, possibly carcinogenic context vs nutritional context.
  • Is the prostate cancer signal in SELECT replicable? No subsequent large RCT has tested. PHS-II was negative for prostate cancer but lower dose. Worth tracking longitudinal data from SELECT participants.
  • 23andMe genotypes worth flagging for vitamin E: APOE (lipoprotein metabolism), CYP4F2 V433M (tocopherol clearance + warfarin interaction), TTPA variants (α-TTP function — rare but meaningful if present).

References

Miller ER 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E. Meta-Analysis: High-Dosage Vitamin E Supplementation May Increase All-Cause Mortality. Ann Intern Med 2005;142:37-46. PMID 15537682

pubmed.ncbi.nlm.nih.gov · 2005

the foundational high-dose mortality signal meta-analysis. Pooled 19 trials, n=135,967; ≥400 IU/day all-rac-α-tocopherol associated with increased all-cause mortality.

View Study

Sanyal AJ, Chalasani N, Kowdley KV, et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med 2010;362:1675-1685. PMID 20427778

pubmed.ncbi.nlm.nih.gov · 2010

PIVENS trial, the foundational NASH evidence supporting AASLD recommendation. RRR-α-tocopherol 800 IU/day for 96 weeks improved histology in non-diabetic biopsy-proven NASH.

View Study

The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994;330:1029-1035. PMID 8127329

pubmed.ncbi.nlm.nih.gov · 1994

ATBC trial. α-tocopherol 50 mg/day no lung cancer reduction; β-carotene arm increased lung cancer.

View Study

Klein EA, Thompson IM Jr, Tangen CM, et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 2011;306:1549-1556. PMID 21990298

pubmed.ncbi.nlm.nih.gov · 2011

SELECT trial. α-tocopherol 400 IU/day increased prostate cancer 17% in healthy men.

View Study

Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease (CARET). N Engl J Med 1996;334:1150-1155. PMID 8602180

pubmed.ncbi.nlm.nih.gov · 1996

CARET trial. β-carotene + retinyl palmitate increased lung cancer in smokers/asbestos workers; trial halted early.

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Ristow M, Zarse K, Oberbach A, et al. Antioxidants prevent health-promoting effects of physical exercise in humans. PNAS 2009;106:8665-8670.

pnas.org · 2009

antioxidant-blunting of training adaptation (E + C 1000 mg/day).

View Source

Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington (DC): National Academies Press; 2000.

ncbi.nlm.nih.gov · 2000

RDA 15 mg/day; tolerable UL 1000 mg/day for adults.

View Source

NIH Office of Dietary Supplements — Vitamin E Fact Sheet for Health Professionals

ods.od.nih.gov

current consensus reference; food sources, RDA, UL, deficiency, supplementation.

View Source

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