Tocotrienols — The Other Vitamin E Family (Palm, Annatto, Rice Bran)

Table of Contents

1. The Eight Vitamin E Isomers
2. Why Tocotrienols Are 40-60× More Potent
3. Sources: Palm, Annatto, and Rice Bran
4. Cardiovascular: HMG-CoA Reductase and Delta-Tocotrienol
5. Liver Health: The Magosso 2013 Non-Alcoholic Fatty Liver Disease Trial
6. Neuroprotection: Alpha-Tocotrienol's Unique Brain Effects
7. Anti-Cancer: Gamma-Tocotrienol in Breast and Pancreatic Cancer
8. Bone, Skin, and Anti-Aging
9. The Alpha-Tocopherol Displacement Problem
10. Doses Used in the Trials
11. Cautions & Drug Interactions
12. Key Research Papers
13. Connections
14. Featured Videos

1. The Eight Vitamin E Isomers

"Vitamin E" is a family name for eight naturally occurring molecules that share a chromanol ring (the antioxidant business end) attached to a 16-carbon side chain. The eight split into two sub-families based on the side chain:

• Tocopherols (4 forms) — saturated phytyl side chain (no double bonds). Alpha, beta, gamma, and delta forms differ by the position and number of methyl groups on the chromanol ring.
• Tocotrienols (4 forms) — unsaturated farnesyl side chain (three double bonds in the tail). Same four methylation patterns: alpha, beta, gamma, delta tocotrienol.

The three double bonds in the tocotrienol tail are the key structural difference. The unsaturated tail is more flexible, lets the molecule penetrate more deeply into the fatty interior of cell membranes, and exposes the active chromanol ring to a wider area — which is why tocotrienols are recycled faster and intercept lipid radicals more efficiently than tocopherols at the same concentration.

The methylation pattern on the chromanol ring matters too. Alpha forms have three methyls (one each at positions 5, 7, and 8). Beta forms have methyls at 5 and 8. Gamma forms have methyls at 7 and 8. Delta forms have only one methyl, at position 8. The fewer the methyls, the more open the position 5 on the ring is for trapping reactive nitrogen species like peroxynitrite — which is why gamma-tocopherol/tocotrienol traps reactive nitrogen species that alpha-forms cannot.

Of the eight, alpha-tocopherol is the one preferentially retained by the liver's alpha-tocopherol transfer protein (α-TTP), incorporated into very-low-density lipoprotein (VLDL), and distributed throughout the body. The other seven are largely metabolized to water-soluble CEHCs (carboxyethyl hydroxychromans) by CYP4F2 and excreted in urine and bile. This is why plasma Vitamin E is mostly alpha-tocopherol — the body actively retains it — but it does NOT mean the other seven forms are unimportant. They simply act locally during their passage through tissues before catabolism.

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2. Why Tocotrienols Are 40-60× More Potent (For Some Indications)

"More potent" is widely repeated about tocotrienols but the headline number depends entirely on the indication. Here is what the literature actually supports:

• Lipid peroxidation in membranes — in a laboratory test on rat liver membranes (microsomes), d-alpha-tocotrienol was 40-60× more effective than d-alpha-tocopherol at preventing iron-driven lipid peroxidation (Serbinova 1991, Free Radical Biology and Medicine). The authors gave three reasons: (1) alpha-tocotrienol is recycled more efficiently from its spent (chromanoxyl radical) form, (2) it spreads more evenly through the membrane bilayer, and (3) it loosens (disorders) the membrane fats more, so it meets fat radicals more easily. The same paper notes that alpha-tocotrienol has only about 30% of alpha-tocopherol's vitamin E activity in the standard vitamin tests.
• Neuroprotection against glutamate excitotoxicity — alpha-tocotrienol protects neurons from glutamate-induced death at nanomolar concentrations (10-50 nM), while alpha-tocopherol requires micromolar concentrations (10-50 μM) for the same effect — a 1000× potency difference in this specific cell-culture assay on HT4 hippocampal neuron cells (Sen 2000, Journal of Biological Chemistry). Sen 2000 traced the effect to blocking the c-Src kinase signal, and a 2003 follow-up (Khanna 2003) to 12-lipoxygenase — signalling effects, not simple antioxidant activity.
• Cholesterol synthesis inhibition — delta-tocotrienol and gamma-tocotrienol post-transcriptionally suppress HMG-CoA reductase (the rate-limiting enzyme of cholesterol synthesis — the same enzyme inhibited by statin drugs). Alpha-tocopherol does NOT do this; it actually antagonizes the tocotrienol cholesterol-lowering effect.
• Apoptosis induction in cancer cells — gamma- and delta-tocotrienol induce apoptosis in breast cancer, pancreatic cancer, and prostate cancer cell lines at micromolar concentrations where alpha-tocopherol is inactive.
• Standard linoleate-radical scavenging — for the basic chemistry of intercepting a peroxyl radical in solution, alpha-tocopherol and alpha-tocotrienol are similar. The "40-60×" advantage shows up only in membrane and cellular contexts where geometry matters.

The honest summary: tocotrienols are NOT a universal "stronger Vitamin E." In laboratory studies they are differently potent for specific effects — much stronger than alpha-tocopherol for neuron protection, cholesterol-enzyme effects and cancer-cell death; comparable for ordinary antioxidant chemistry. The research on these specific effects used gamma- and delta-tocotrienol (as in annatto extracts) and mixed palm tocotrienols; the mixed tocopherols in whole nuts and seeds supply most of the vitamin E in ordinary diets.

What is not known: the 40-60× figure comes from rat liver membranes and the 1000× figure from neuron cells grown in a dish. No human trial on this page shows that tocotrienols are stronger than alpha-tocopherol in people.

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3. Sources: Palm, Annatto, and Rice Bran

Tocotrienols are uncommon in the typical Western diet. Sunflower oil, soybean oil, corn oil, almonds — all the standard "Vitamin E" foods — provide almost exclusively tocopherols, not tocotrienols. The three concentrated dietary sources are:

• Palm oil (red palm fruit) — contains a mixed tocotrienol fraction (TRF) of approximately 70% tocotrienols and 30% tocopherols. The four tocotrienols (alpha, beta, gamma, delta) are all present, with alpha and gamma typically the most abundant. Palm tocotrienol-rich fraction (Palm TRF) is the source for most cardiovascular and liver clinical trials. Certified sustainable palm oil is also sold.
• Annatto seeds (Bixa orellana) — produces a tocotrienol extract that is approximately 90% delta-tocotrienol and 10% gamma-tocotrienol, with virtually NO tocopherols. This near-pure tocotrienol profile is the form used in research where the alpha-tocopherol displacement effect matters (cancer-prevention research, cholesterol studies). Commercial forms include an annatto-derived delta-tocotrienol product and, from palm, a self-emulsifying palm tocotrienol complex.
• Rice bran oil — contains modest amounts of all four tocotrienols along with gamma-oryzanol (a separate cholesterol-modulating compound). The total tocotrienol content per gram is lower than palm or annatto, but the dietary use of rice bran oil in Asian cuisines provides meaningful cumulative intake.

Other minor sources include barley, oats, and certain wheat varieties (containing primarily alpha-tocotrienol), and some emerging interest in coconut oil byproducts. None of these reach the concentrations of palm or annatto.

The U.S. dietary intake of total tocotrienols is estimated at <5 mg/day for most adults — far below the 100-400 mg/day of tocotrienols given as supplements in the trials discussed below.

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4. Cardiovascular: HMG-CoA Reductase and Delta-Tocotrienol

The single most distinctive cardiovascular mechanism of tocotrienols is post-transcriptional inhibition of HMG-CoA reductase — the rate-limiting enzyme in cholesterol synthesis. Statin drugs (atorvastatin, rosuvastatin, simvastatin) competitively inhibit the active site of this enzyme. Tocotrienols work upstream: they accelerate the degradation of the enzyme protein itself, reducing the total amount of HMG-CoA reductase in the cell.

• Delta-tocotrienol is the most potent for this effect, followed by gamma-tocotrienol. Alpha-tocotrienol is weaker. Alpha-tocopherol does NOT inhibit HMG-CoA reductase — and in a 1996 feeding study in chickens, adding alpha-tocopherol to a gamma-tocotrienol blend weakened the tocotrienol's effect on the enzyme (Qureshi 1996, Journal of Nutrition).
• Clinical effects — early small studies reported falls in cholesterol: in Qureshi's 1991 pilot crossover study, 200 mg/day of palm tocotrienol capsules for 4 weeks lowered total cholesterol 15% and low-density lipoprotein (LDL) cholesterol 8%, and in Qureshi's 2001 study of 28 people with high cholesterol, 50 mg/day of a rice-bran tocotrienol fraction with a heart-healthy diet lowered total cholesterol 14% and LDL 18%. Pooled results do not confirm this: a 2020 meta-analysis of 15 randomized trials (20 treatment arms) found that tocotrienols did not significantly change total cholesterol, LDL cholesterol or triglycerides, while HDL ("good") cholesterol rose slightly (by 0.146 mmol/L), more so at doses of 200 mg/day or more (Zuo 2020). Statin drugs lower LDL by 30-50%.
• Anti-platelet effects — tocotrienols reduce platelet aggregation through similar mechanisms as tocopherols (PKC inhibition, thromboxane reduction).
• Endothelial function — tocotrienols improve nitric oxide bioavailability and reduce inflammatory adhesion molecule expression on vascular endothelium.
• Carotid atherosclerosis regression — the Tomeo 1995 trial (small, 50 patients with narrowed neck arteries, a palm tocotrienol and alpha-tocopherol fraction for 18 months) measured the arteries by duplex ultrasound: 7 of the 25 tocotrienol patients showed apparent narrowing regression and 2 progression, while none of the 25 controls showed regression and 10 progressed (P < 0.002). Total cholesterol, LDL cholesterol and triglycerides stayed unchanged in both groups. The trial was small and has not been definitively replicated, but suggests tocotrienols may affect plaque biology through a route other than cholesterol lowering.

In Qureshi's 2001 study, the rice-bran tocotrienol fraction combined with 10 mg/day of lovastatin lowered total cholesterol 20% and LDL 25%, and no participant reported side effects over 25 weeks. Larger trials of the combination are lacking, and the 2020 meta-analysis found no significant LDL change from tocotrienols overall.

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5. Liver Health: The Magosso 2013 Non-Alcoholic Fatty Liver Disease Trial

Non-alcoholic fatty liver disease (NAFLD) is now the most common chronic liver disease worldwide, driven primarily by metabolic syndrome, insulin resistance, and dietary fructose. On March 14, 2024 the U.S. Food and Drug Administration approved resmetirom, the first drug for adults with the inflammatory form of the disease (non-alcoholic steatohepatitis) with moderate to advanced liver scarring but no cirrhosis, to be used along with diet and exercise (FDA announcement). In 2023 a multisociety consensus of liver societies renamed non-alcoholic fatty liver disease "metabolic dysfunction-associated steatotic liver disease" (MASLD) (Rinella 2023). Both alpha-tocopherol (the PIVENS trial, 800 international units (IU)/day) and tocotrienols (multiple smaller trials) have evidence for benefit.

The pivotal tocotrienol trial is Magosso et al. 2013 (Nutrition Journal): 87 untreated adults with high cholesterol and ultrasound-proven fatty liver, randomized to mixed palm tocotrienols 200 mg twice daily (400 mg/day total) or placebo for 12 months. Primary outcome: ultrasound remission of hepatic steatosis.

• In the main analysis of all 87 people enrolled (intention to treat), 34.9% of the tocotrienol group (15 of 43) reached a normal liver ultrasound versus 18.2% on placebo (8 of 44) (P = 0.039)
• Among completers only (the 64 people who finished the year), the figures were 50.0% (15 of 30) versus 23.5% (8 of 34) (P = 0.014); the fatty liver grade worsened in two placebo patients and in none on tocotrienols
• Blood tests — including the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) — showed no statistically significant difference between the groups from start to finish (full text, Table 5)
• No adverse events were reported in either group
• The required duration was long (12 months) — consistent with how slowly steatosis resolves on any intervention

Mechanism: tocotrienols address non-alcoholic fatty liver disease through multiple pathways simultaneously — reduced lipid peroxidation in hepatocyte membranes, inhibition of HMG-CoA reductase (reducing intrahepatic cholesterol burden), Nrf2 pathway activation (upregulating endogenous antioxidant enzymes), reduction of tumor necrosis factor-alpha and inflammatory cytokine signaling, and modest improvement of insulin sensitivity. This multimodal action is well-suited to a multifactorial disease like non-alcoholic fatty liver disease.

A 2022 randomized double-blind trial in Pakistan (Pervez 2022) compared delta-tocotrienol 300 mg with alpha-tocopherol 268 mg, each twice daily for 48 weeks, in 100 people with non-alcoholic fatty liver disease. Both groups improved equally in liver fat (fatty liver index and computed tomography liver-to-spleen ratio), insulin resistance and the oxidative-stress marker malondialdehyde. Delta-tocotrienol lowered body weight, the inflammation markers interleukin-6 and tumor necrosis factor-alpha, leptin and the liver-cell-death marker cytokeratin-18 more, and raised adiponectin more. No adverse events were reported.

For biopsy-proven non-alcoholic steatohepatitis (NASH) (the inflammatory advanced form of non-alcoholic fatty liver disease), conventional guidance has listed alpha-tocopherol 800 international units/day based on the PIVENS trial (men and post-menopausal women; not people with diabetes, because of a mortality signal in some analyses). Tocotrienols have been compared head-to-head with alpha-tocopherol in one trial so far (Pervez 2022, above).

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6. Neuroprotection: Alpha-Tocotrienol's Unique Brain Effects

Alpha-tocotrienol is the most-studied neuroprotective tocotrienol, with effects mediated through mechanisms independent of and additive to its antioxidant activity. Chandan Sen and colleagues at Ohio State (and later at Indiana) have published most of the foundational work.

• 12-Lipoxygenase inhibition — alpha-tocotrienol inhibits 12-lipoxygenase, the enzyme that produces 12-HPETE (a lipid signaling molecule that drives glutamate-induced neuron death in stroke). Alpha-tocopherol does NOT inhibit 12-LOX. This is why alpha-tocotrienol protects neurons against glutamate excitotoxicity at nanomolar concentrations while alpha-tocopherol fails at micromolar concentrations.
• c-Src kinase suppression — alpha-tocotrienol blocks c-Src activation in neurons, another non-antioxidant signaling effect relevant to stroke and traumatic brain injury.
• Stroke models — in canine and primate stroke models, alpha-tocotrienol supplementation before middle cerebral artery occlusion significantly reduces infarct volume and improves functional outcomes. The effect persists when supplementation begins before the stroke; post-stroke initiation has been less consistently studied.
• White matter preservation — supplementation studies in healthy adults using diffusion tensor imaging have shown that tocotrienol supplementation may slow the age-related decline in cerebral white matter integrity.
• Cognitive effects in older adults — small trials of mixed tocotrienol supplementation in cognitively healthy older adults have suggested modest improvements in some cognitive domains, though larger and longer trials are needed.

Most of the neuroprotection evidence above comes from cell and animal studies. It concerns alpha-tocotrienol, which mixed palm tocotrienols contain; annatto extracts are mostly delta-tocotrienol and contain very little alpha-tocotrienol, the most neuroprotective form in these studies.

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7. Anti-Cancer: Gamma-Tocotrienol in Breast and Pancreatic Cancer

The anti-cancer literature on tocotrienols is large in preclinical (cell culture and animal) work but limited in human trial data. The most-developed indications:

• Breast cancer — gamma-tocotrienol and delta-tocotrienol induce apoptosis in estrogen-receptor positive and triple-negative breast cancer cell lines through multiple mechanisms (caspase activation, NF-kB inhibition, downregulation of survival proteins like Bcl-2). The Nesaretnam group (Malaysian Palm Oil Board) has published most of this work. A 5-year double-blind, placebo-controlled pilot trial in 240 women with early, estrogen-receptor-positive breast cancer added palm tocotrienol-rich fraction or placebo to tamoxifen (the women were not randomly assigned). Five-year disease-free survival was 86.7% versus 83.3%, a difference that was not statistically significant, and the authors concluded there "seems to be no association" between tocotrienol and breast-cancer survival (Nesaretnam 2010).
• Pancreatic cancer — delta-tocotrienol has been investigated as an adjunct to gemcitabine in pancreatic cancer. The mechanism is sensitization of resistant pancreatic cancer cells to chemotherapy through NF-kB pathway inhibition. A Phase I trial established safety; Phase II efficacy data are emerging.
• Prostate cancer — given the SELECT trial's signal that alpha-tocopherol monotherapy may increase prostate cancer risk, there is interest in whether the other Vitamin E forms (especially gamma-tocopherol and tocotrienols) might do the opposite. Preclinical data are encouraging; large human trials are not yet available.
• Radiation protection — gamma-tocotrienol has been investigated by the U.S. military as a potential radiation countermeasure (for nuclear accident scenarios). Animal studies show it protects hematopoietic stem cells from radiation injury when given before radiation exposure.

Some chemotherapy agents (cisplatin, doxorubicin) rely partly on oxidative stress for their cell-killing effect, and antioxidants such as tocotrienols might theoretically interfere. The interaction in practice is unclear and likely depends on the specific chemotherapy and tumor type.

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8. Bone, Skin, and Anti-Aging

• Bone health — tocotrienols (particularly gamma and delta) have shown bone-preserving effects in ovariectomized rat models of postmenopausal osteoporosis. They appear to upregulate osteoblast (bone-forming cell) activity and downregulate osteoclast (bone-resorbing cell) activity. Human trial data are emerging from Malaysia.
• Skin photoaging — tocotrienols penetrate the stratum corneum more effectively than tocopherols when applied topically, and reach deeper skin layers. Topical tocotrienol formulations are part of a small but growing dermatological literature on alternative Vitamin E sources for photoaging.
• Hair growth — a small placebo-controlled trial (Beoy 2010, Penang) in volunteers with hair loss gave 21 people 100 mg/day of mixed tocotrienols and 17 people a placebo for 8 months: hair count in a marked scalp area rose 34.5% in the tocotrienol group and fell 0.1% on placebo, while the weight of hair strands did not differ. One author worked for a supplement manufacturer. Replication is needed.
• Anti-aging mechanism — the overall picture is that tocotrienols favorably affect multiple aging-related pathways: Nrf2-driven antioxidant gene expression, mitochondrial function, inflammatory cytokine reduction, and lipid peroxidation in cell membranes. Whether this translates to a measurable longevity effect in humans is not established.

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9. The Alpha-Tocopherol Displacement Problem

A critical point that explains why much of the historical "Vitamin E" trial literature is misleading: high-dose alpha-tocopherol supplementation actively reduces the body's gamma-tocopherol and tocotrienol levels.

Three mechanisms drive this:

1. Liver alpha-TTP saturation — the alpha-tocopherol transfer protein in the liver preferentially binds and recirculates alpha-tocopherol. Flooding the system with supplemental alpha-tocopherol saturates alpha-TTP and accelerates the catabolism of all the non-alpha forms (gamma-tocopherol, delta-tocopherol, all four tocotrienols) by CYP4F2.
2. Plasma displacement — alpha-tocopherol supplementation at 400-1000 international units/day reduces plasma gamma-tocopherol by 30-50% within weeks.
3. Direct antagonism at HMG-CoA reductase — for the cholesterol-lowering mechanism specifically, alpha-tocopherol at high concentrations interferes with the tocotrienol effect on enzyme degradation.

This is why the HOPE, SELECT, and similar large alpha-tocopherol-only trials produced flat or negative results despite the strong biological plausibility of "antioxidants prevent cardiovascular disease." The supplementation regimen actively depleted the very forms (gamma-tocopherol, tocotrienols) that probably do most of the protective work in a normal mixed-tocopherol diet.

These findings are the reason some researchers favor mixed-tocopherol + tocotrienol formulations over alpha-tocopherol alone. The forms on the market fall into three groups:

• Mixed tocopherols (alpha + beta + gamma + delta) without tocotrienols — e.g. a mixed tocopherol supplement
• Annatto tocotrienols (90% delta + 10% gamma, no tocopherols) — e.g. an annatto-derived delta-tocotrienol product
• Palm tocotrienol-rich fraction (TRF) — mixed tocotrienols + some tocopherols — the form used in most cardiovascular and non-alcoholic fatty liver disease trials

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10. Doses Used in the Trials

The doses below are the ones used in the studies described on this page.

Doses in the studies

• Fatty liver: Magosso 2013 gave mixed palm tocotrienols 200 mg twice daily (400 mg/day total) for 1 year; Pervez 2022 gave delta-tocotrienol 300 mg twice daily for 48 weeks.
• Cholesterol: Qureshi 1991 gave 200 mg/day of palm tocotrienol capsules; Qureshi 2001 gave 50 mg/day of a rice-bran tocotrienol fraction. In the 2020 meta-analysis, the HDL rise was larger at 200 mg/day or more.
• Carotid arteries: Tomeo 1995 gave a palm tocotrienol fraction for 18 months.
• Hair loss: Beoy 2010 gave mixed tocotrienols 100 mg/day for 8 months.
• Neuroprotection: the brain findings come mostly from cell and animal studies, which contain alpha-tocotrienol; annatto provides almost no alpha-tocotrienol.

Timing & absorption

• Tocotrienols are fat-soluble, and absorption from an empty stomach is poor; practitioners describe taking them with a meal containing fat (15+ grams).
• Separation times sometimes given — 8+ hours from iron supplements and 12+ hours from high-dose alpha-tocopherol — are not tested in any trial on this page; the alpha-tocopherol concern comes from the displacement findings in section 9.

What the trials measured

• Cholesterol studies measured the blood lipid panel (total, LDL and HDL cholesterol, triglycerides).
• Magosso 2013 measured abdominal ultrasound plus blood tests including aspartate aminotransferase, alanine aminotransferase and gamma-glutamyl transferase (GGT).
• The bleeding concern with warfarin, antiplatelet drugs and surgery is set out in section 11.

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11. Cautions & Drug Interactions

• Warfarin and antiplatelet drugs — tocotrienols, like tocopherols, have mild anti-platelet effects. This can add to the effect of warfarin and antiplatelet drugs; the international normalized ratio (INR, the warfarin blood test) shows the change, and some clinicians check it more often in the first 4 weeks.
• Statins — in Qureshi's 2001 study, a rice-bran tocotrienol fraction with lovastatin lowered LDL more than either alone; there are no large trials of the combination.
• Chemotherapy — tocotrienols may sensitize some tumors to chemotherapy but could theoretically interfere with the oxidative-stress component of others.
• Surgery — because of the mild anti-platelet effect, surgeons commonly ask for vitamin E supplements to be stopped about 2 weeks before elective surgery.
• Pregnancy and breastfeeding — there is no good safety data on high-dose tocotrienol supplements during pregnancy and breastfeeding.
• Annatto allergy — annatto-derived tocotrienols are theoretically a concern for the rare individuals with annatto/bixin food coloring allergy.
• Gastrointestinal (GI) side effects — nausea, bloating, or loose stools occur in a small minority. People report this usually settles when taken with a larger meal.
• Drug interactions — the literature is much smaller for tocotrienols than for alpha-tocopherol. The interactions known for vitamin E in general (anticoagulants, antiplatelets, fish oil, vitamin K) are the best guide available; tocotrienol-specific data are scarce.

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Key Research Papers

1. Serbinova E, Kagan V, Han D, Packer L (1991). Free radical recycling and intramembrane mobility in the antioxidant properties of alpha-tocopherol and alpha-tocotrienol. Free Radical Biology and Medicine. — PubMed PMID: 1649783
2. Sen CK et al. (2000). Molecular basis of vitamin E action: tocotrienol potently inhibits glutamate-induced pp60(c-Src) kinase activation and death of HT4 neuronal cells. Journal of Biological Chemistry. — PubMed PMID: 10777609
3. Qureshi AA et al. (1991). Lowering of serum cholesterol in hypercholesterolemic humans by tocotrienols (palmvitee). American Journal of Clinical Nutrition. — PubMed PMID: 2012010
4. Qureshi AA, Pearce BC, Nor RM, Gapor A, Peterson DM, Elson CE (1996). Dietary alpha-tocopherol attenuates the impact of gamma-tocotrienol on hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in chickens. Journal of Nutrition. — PubMed PMID: 8632210
5. Qureshi AA et al. (2001). Synergistic effect of tocotrienol-rich fraction (TRF(25)) of rice bran and lovastatin on lipid parameters in hypercholesterolemic humans. Journal of Nutritional Biochemistry. — PubMed PMID: 11516635
6. Zuo S, Wang G, Han Q, Xiao H, O Santos H, Avelar Rodriguez D, Khani V, Tang J (2020). The effects of tocotrienol supplementation on lipid profile: A meta-analysis of randomized controlled trials. Complementary Therapies in Medicine. — PubMed PMID: 32951713
7. Magosso E et al. (2013). Tocotrienols for normalisation of hepatic echogenic response in nonalcoholic fatty liver: a randomised placebo-controlled clinical trial. Nutrition Journal. — PubMed PMID: 24373555
8. Pervez MA, Khan DA, Mirza SA, Slehria AUR, Nisar U, Aamir M (2022). Comparison of delta-tocotrienol and alpha-tocopherol effects on hepatic steatosis and inflammatory biomarkers in patients with non-alcoholic fatty liver disease: A randomized double-blind active-controlled trial. Complementary Therapies in Medicine. — PubMed PMID: 35933083
9. Rinella ME, Lazarus JV, Ratziu V, et al. (2023). A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology. — PubMed PMID: 37363821
10. Tomeo AC et al. (1995). Antioxidant effects of tocotrienols in patients with hyperlipidemia and carotid stenosis. Lipids. — PubMed PMID: 8614310
11. Khanna S et al. (2003). Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegeneration. Journal of Biological Chemistry. — PubMed PMID: 12917400
12. Nesaretnam K et al. (2004). Tocotrienol-rich fraction from palm oil and gene expression in human breast cancer cells. Annals of the New York Academy of Sciences. — PubMed PMID: 15753141
13. Nesaretnam K, Selvaduray KR, Abdul Razak G, Veerasenan SD, Gomez PA (2010). Effectiveness of tocotrienol-rich fraction combined with tamoxifen in the management of women with early breast cancer: a pilot clinical trial. Breast Cancer Research. — PubMed PMID: 20929592
14. Springett GM et al. (2015). A Phase I safety, pharmacokinetic, and pharmacodynamic presurgical trial of vitamin E delta-tocotrienol in patients with pancreatic ductal neoplasia. EBioMedicine. — PubMed PMID: 26844278
15. Sen CK, Khanna S, Roy S (2004). Tocotrienol: the natural vitamin E to defend the nervous system? Annals of the New York Academy of Sciences. — PubMed PMID: 15753140
16. Beoy LA, Woei WJ, Hay YK (2010). Effects of tocotrienol supplementation on hair growth in human volunteers. Tropical Life Sciences Research. — PubMed PMID: 24575202
17. Aggarwal BB et al. (2010). Tocotrienols, the vitamin E of the 21st century: its potential against cancer and other chronic diseases. Biochemical Pharmacology. — PubMed PMID: 20696139
18. Patel V et al. (2012). Oral tocotrienols are transported to human tissues and delay the progression of the model for end-stage liver disease score in patients. Journal of Nutrition. — PubMed PMID: 22298568

PubMed Topic Searches

1. PubMed: Tocotrienols and HMG-CoA reductase
2. PubMed: Delta-tocotrienol (annatto)
3. PubMed: Alpha-tocotrienol and neuroprotection
4. PubMed: Palm tocotrienol-rich fraction (TRF)
5. PubMed: Tocotrienols and NAFLD
6. PubMed: Gamma-tocotrienol and breast cancer
7. PubMed: Tocotrienols and pancreatic cancer
8. PubMed: Tocotrienols and bone health
9. PubMed: Tocotrienols and radiation protection
10. PubMed: Alpha-tocopherol displacement of tocotrienols
11. PubMed: Mixed tocopherol + tocotrienol supplementation
12. PubMed: Rice bran oil and tocotrienols

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Connections

• All Vitamins
• Vitamin E (Main Page)
• Vitamin E Benefits Hub
• Vitamin E and Heart Health
• Vitamin E and Immune Function
• Vitamin E and Skin Health
• Cardiovascular Disease
• Atherosclerosis
• Stroke
• Non-Alcoholic Fatty Liver Disease / Non-Alcoholic Steatohepatitis
• Cancer
• Stroke
• Vitamin C
• Vitamin A
• Selenium
• Oxidative Stress
• Olive Oil
• Almonds
• Tocotrienols — the dedicated antioxidant page for this half of the Vitamin E family.
• Deficiency
• Toxicity
• History
• Sources

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