Vitamin E is the most important fat-soluble antioxidant in food and consists of eight related vitamin E compounds (together called vitamin E complex): four tocopherols (α-, β-, γ-, and δ-tocopherol) and four tocotrienols (α-, β-, γ-, and δ-tocotrienol). In addition to its antioxidant activity, vitamin E influences cell signaling and gene expression. These functions may be even more important for health and disease prevention/progression than direct antioxidant activity. 

Source: Orthokennis

Vitamin E combats aging processes (including atherosclerosis and inflamm-aging), supports metabolism, is essential for fertility, and supports the health of various systems including the heart and blood vessels, immune system, nervous system, bones, muscles, liver, skin, hair, and eyes.

Sources

Plant oils, nuts, seeds, fatty fish, eggs, whole grains, vegetables (including spinach), and fruit.

Quality aspects

When supplementing with vitamin E, it is better to choose a supplement containing all 8 vitamin E compounds. Each vitamin E compound has unique properties, and vitamin E compounds enhance each other's effects (synergy). One-sided supplementation with α-tocopherol reduces the concentrations of other vitamin E compounds (including γ-tocopherol and α-tocotrienol), reducing the body's ability to benefit from the health effects of the full vitamin E complex. It is also important to choose natural vitamin E (RRR-stereo-isomers) rather than the synthetic variant. Natural vitamin E is much more effective; a significant portion of synthetic stereo-isomers have no biological activity and may even burden the body.

Signs of possible deficiency

Anemia, reduced immunity, neuromuscular and neurological symptoms including ataxia, AVED (ataxia with vitamin E deficiency).

Indications for increased vitamin E requirement include fat malabsorption (cystic fibrosis, cholestasis, celiac disease), endurance sports, and metabolic syndrome inhibition of aging, improvement of quality of life in the elderly atherosclerosis, cardiovascular diseases (especially prevention) liver diseases (non-alcoholic fatty liver, steatohepatitis, hepatitis B, hepatitis C, acute liver failure) (early stages) age-related macular degeneration (prevention) cataracts (prevention) neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, ALS (amyotrophic lateral sclerosis) cyclic mastalgia menstrual pain (dysmenorrhea) PCOS (polycystic ovary syndrome) reduced fertility menopausal symptoms diabetes mellitus (type 1 and 2), diabetes complications (neuropathy, nephropathy, retinopathy, diabetic foot) (prevention) COPD (prevention) osteoporosis (prevention) sarcopenia chronic kidney disease, hemodialysis

Contraindications

Hypersensitivity to vitamin E Pregnancy and breastfeeding (except for vitamin E in a (pregnancy) multivitamin)

Usage advice

General maintenance dose of vitamin E (complex)*: 100-200 mg-TE per day General therapeutic dose of vitamin E (complex)**: 100-600 mg-TE per day (or even higher, especially in neurodegenerative diseases) Chronic liver diseases: 400-1200 mg-TE per day

*The amount of vitamin E (complex) is expressed in mg-TE (mg d-alpha-tocopherol equivalents), IU (international units), or mg (of the respective vitamin E compound): 1 mg α-tocopherol (natural) = 1 mg TE = 1.49 IU 1 mg α-tocopherol (synthetic) = 0.735 mg-TE = 1 IU 1 mg β-tocopherol (RRR) = 0.5 mg-TE 1 mg γ-tocopherol (RRR) = 0.1 mg-TE 1 mg δ-tocopherol (RRR) = 0.03 mg-TE 1 mg α-tocotrienol = 0.3 mg-TE 1 mg β-tocotrienol = 0.05 mg-TE

**High doses of vitamin E are preferably used for a limited period. The safety of chronic intake of vitamin E in doses above 400 mg-TE per day has been under discussion in recent years. Doses should be gradually increased and decreased. Ensure an adequate intake of antioxidants that recycle oxidized vitamin E such as vitamin C.

Interactions

Tocotrienols can prolong bleeding and clotting time. More research is needed in this area. When using anticoagulants, caution is advised with the intake of a supplement containing tocotrienols. A high dose of α-tocopherol (1000 IU natural α-tocopherol) antagonizes vitamin K and increases PIVKA II (non-carboxylated prothrombin) in adults not using anticoagulants (mild anticoagulant effect). Adequate intake of vitamin K(2) is important with vitamin E supplementation. People using vitamin K antagonists should not take more than 800 IU of α-tocopherol per day (preferably no more than 400 IU/day). There is evidence that vitamin E supplementation increases the risk of bleeding in people using aspirin, possibly because aspirin can lower the vitamin K status. Oxidized vitamin E (which has pro-oxidant activity) is recycled by other antioxidants including vitamin C and coenzyme Q10. Adequate intake of these synergists is important with vitamin E supplementation. A high dose of α-tocopherol can increase the activity of CYP3A4 (and possibly other cytochrome P450 enzymes), reducing the effectiveness of medications metabolized by this enzyme (animal studies). The clinical relevance of this needs further investigation. Carbamazepine, phenytoin, phenobarbital, and orlistat can lower the vitamin E status; vitamin E supplementation may be desired. Alpha-tocopherol in doses from 800 IU/day can greatly reduce the absorption of beta-carotene. Vitamin E may protect against contrast-induced acute kidney injury. Lipid-lowering medications such as statins reduce vitamin E concentration in blood and tissues. Statin-induced reduction in vitamin E status may play a role in statin-induced myopathy. Vitamin E protects against peripheral neuropathy induced by cytostatics (including paclitaxel and cisplatin). Tocotrienols and lovastatin have a synergistic cholesterol-lowering effect. Vitamin E may slow the progression of tardive dyskinesia caused by antipsychotics. The combination of vitamin E and omega-3 fatty acids protects dose-dependently against cardiovascular damage induced by fine particulate matter (PM2.5: particles with a diameter smaller than 2.5 micrometers) (animal study). Vitamin E protects kidneys, liver, brain, and testes against heavy metal toxicity such as lead, mercury, cadmium, aluminum, silver, and copper (animal studies). Vitamin E protects against neurotoxicity of THC (delta-9-tetrahydrocannabinol, a component in cannabis) and PCBs (polychlorinated biphenyls, a group of highly toxic organic chlorine compounds). PCBs lower vitamin E status. Vitamin E (in combination with vitamin C) prevents hemolytic anemia induced by ribavirin. Vitamin E and vitamin C protect against nephrotoxicity of gentamicin and cisplatin (animal studies). Vitamin E protects against lead-induced memory and learning problems (animal study).

Safety

Vitamin E has low toxicity. Use of a (high-dose) vitamin E supplement sometimes causes (nonspecific) symptoms such as nausea, diarrhea, fatigue, muscle weakness, or headache. It is unlikely that α-tocopherol causes bleeding at doses up to 800 IU/day (or 537 mg α-TE/day), even in people using anticoagulants. It is advisable to avoid (very) high doses of vitamin E (from 800 mg α-TE/day) for 2 weeks before surgery. Various meta-analyses indicate that a vitamin E intake from 400 IU/day increases the risk of death by 3%. This may apply especially to people with cardiovascular diseases. However, other meta-analyses conclude that supplementation with vitamin E in doses up to 5500 IU/day does not lead to an increased risk of death. The upper limit (UL) for (prolonged) intake of vitamin E (α-tocopherol) is: 1-3 years: 100 mg/day 4-6 years: 120 mg/day 7-10 years: 160 mg/day 11-14 years: 220 mg/day 15-17 years: 260 mg/day from 18 years: 300 mg/day In the United States, a UL for (healthy) adults of 1000 mg/day (1500 IU natural α-tocopherol) applies.