Facts, Articles, Research

What the science says (1990–2026): Vitamin E

These citations support correction of deficiency, specified forms, and elemental amounts — the same logic used in MD's Choice formulas. They are not claims that a supplement treats disease.

Alpha-Tocopherol Beta-Carotene 1994; SELECT 2008; 2022–2024 antioxidant reviews. Vitamin E is an essential fat-soluble antioxidant. High-dose synthetic alpha-tocopherol trials did not prevent cancer or heart disease in already-nourished adults.

These products are not intended to diagnose, treat, cure, or prevent disease. Historic monograph text below is kept for the original library.

Vitamin E

I. Chemistry

Natural vitamin E includes eight vitamers in two classes
1. The tocols have saturated side chains
2. The tocotrienols have unsaturated side chains
3. Each class is composed of four vitamers which differ in number and location of methyl groups on the phenyl ring
Physical properties
1. Lipid soluble
2. Colorless liquid at room temperature

II. Absorption and Transport of Vitamin E

Absorption of vitamin E is dependent on normal fat absorption
Esters are hydrolyzed to the alcohol in the intestine
Both bile salts and pancreatic juice are needed for the vitamin to diffuse through the enterocyte membrane
Average absorption is 50-70% but the efficiency falls with high intake
Absorbed tocopherol is incorporated into chylomicrons and transported
Tocopherol is distributed to the tissues primarilyy by low-density lipoproteins
Uptake of vitamin E into cells
1. LDL receptor - mediated uptake
2. Lipoprotein lipase-mediated hydrolysis of chylomicrons and very low density lipoproteins.
3. Possibly by other mechanisms
Within the cell cytoplasm and other parts of cells, vitamin E appears to bind to tocopherol-binding proteins for transport
In membranes, the vitamin is likely to be oriented with the phenyl head toward the surface of the membrane near the phosphate region of the phospholipid and the hydrophobic hydroxyl tail buried within the hydrocarbon region
Adipose tissue is a major storage site
1. Concentration in adipose tissue increases linearly with vitamin E intake
2. Other tissues increase very slowly or not at all
3. When intake is low, withdrawal of vitamin E is slow from adipose tissue and rapid from liver and plasma
4. Vitamin E is part of the antioxidant system which protects animals against reactive oxygen molecules and their toxic products. The system contains at least five levels of mechanisms working in concert. Included are protective (levels 1-3), chain breaking (level 4) and toxic product removal (level 5) mechanisms
  1. Enzymes convert superoxide (0₂^-) and hydrogen peroxide (HOOH) produced in normal metabolism and increased by xenobiotics into forms which do not react with catalytic iron. Conversion of 0₂^- to HOOH is accelerated by superoxide dismutases, enzymes which require copper and zinc (in the cytoplasm) or manganese (in membranes). Hydrogen peroxide, in turn, is broken down to water by glutathione peroxidase, a selenium enzyme. Glutathione peroxidase as well as catalase, an iron enzyme, also convert organic hydroxeroxides to less harmful forms
  2. Iron is oxidized to less reactive forms and safely complexed away from catalytic reactions which produce more reactive oxidants. Ceruloplasmin (copper) maintains iron in the less reactive Fe⁺³form. Transferrin and lactoferrin prevent iron from promoting peroxide decomposition or initiating hydroxyl radical (·OH) production by compartmenting it safely away from potential reactions. Certain endogenous materials such as creatine bind metals and prevent indiscriminate coordination of proteins by Cu⁺¹ and possibly Fe⁺² which can initiate ·OH and oxidize the protein
  3. Important molecules may be protected against catalytic iron by zinc which has an outer electron makeup similar to Fe⁺² but is not involved in electron transfer. Zinc may protect against decompartmentalized iron by masking labile sulfur groups and competing for molecular binding sites
  4. Antioxidant molecules terminate ·OH and peroxidative chain reactions initiated by O₂ and HOOH which escape enzymatic control (level 1) and catalytic iron which escapes levels 2 and 3. It is here that lipid soluble vitamin E acts to quench ·OH as it is produced and to interrupt peroxidative chains initiated by ·OH which escape other antioxidant control. Other lipid soluble antioxidant molecules include ubiquinone and b-carotene. Water soluble antioxidant molecules include ascorbate, phenolics, and urate. Vitamin E stabilizes reactive oxygen materials by giving up an electron, itself becoming a radical but with reactivity too low to continue the chain. When vitamin E is inadequate, however, glutathione -S-- transferases conjugate reactive oxygen metabolites with GSH. Since GSH is consumed by this process, rather than merely reversibly oxidized, it is much more efficient for vitamin E to serve as a chain breaker and for GSH to serve as a cofactor for glutathione peroxidase. Vitamin E and GSH can be regenerated by ascorbate which also can act directly as a water soluble antioxidant
  5. Aldehyde dexydrogenases convert toxic aldehydes produced when peroxidized lipids decompose into less harmful products. An example is xanthine dehydrogenase which also helps keep iron in the less reactive ferric form, thereby conserving reducing equivalents, vitamin E, and other chain-breaking antioxidants

III. Other functions of vitamin E related to its antioxidant ability

Prevention of various forms of organ degeneration
1. Prevention of oxidative damage
2. Prevention of accumulation of ceroid pigment granules
  1. Occur in central nervous system, lungs kidneys, adipocytes, and muscle
  2. Contain oxidized unmetabolized lipids that have partially cross linked with peptides to form a hard granule the body cannot dispose of
  3. Such granules may contribute to aging
  4. Accumulation is inhibited by high vitamin E intake
3. Delaying initiation of atherosclerosis and heart disease
  1. Regulating arachidonic acid metabolism and thromboxane production by blood platelets
  2. Protecting low density lipoprotein and cholesterol from oxidation
Roles in male and female reproduction (seen primarilyy in rat and mouse)
1. In male, a deficiency causes degeneration of the seminiferous epithelium which results in cessation of sperm production
2. In female, a failure of uterine development which prevent implantation of the conceptus in uterine walls
Suppression of fecal mutagens within the intestinal tract, especially the colon

IV. Recommended Allowances of Vitamin E

	IU/KgDM
Chick Pig Dairy Cattle Growing heifers Cows Human	10 11 24 15 15 IU/day

V. Interactions with Se, polyunsaturated fatty acids, and sulfur amino acids

Glutathione peroxidase has a vitamin E sparing effect
1. Selenium enzyme
2. Sulfur amino acids needed for glutathione, the specific donor of reducing equivalents for glutathione peroxidase
Glutathione also spares vitamin E by serving as a chain breaker
PUFA's are readily oxidized, so consumption of vitamin E is increased

VI. Vitamin E Deficiency

The only clear cut symptom of vitamin E deficiency in adult humans is increased fragility of red cell membranes
Muscular dystrophy in chick, lamb, calf, pig and rat
Subcutaneous exudates in chick and pig
Liver necrosis in pig and rat
Encephalomacia ill chick, mild neuronal degeneration in rat, monkey, possibly human
Elevation of serum enzymes in chick, pig, lamb
Fetal resorption, testicular degeneration in rat, mice
Incisor depigmentation in rat and mice
Ceroid pigments in rat, yellow fat in pigs
Vitamin E deficiency conditions in relation to selenium
1. Prevented by adequate selenium - muscle degeneration, exudates, liver necrosis
2. Not prevented by selenium - hemolysis, fetal resorption, testicular degeneration, ceroid pigments

VII. Vitamin E and Health Problems

Adequate vitamin E appears to reduce incidences of retained fetal membranes and udder edema in dairy cows
Malabsorption of fat may lead to vitamin E deficiency
The theory that high doses of vitamin E may inhibit the aging process has not been substantiated
1. Ceroid pigment formation can be reduced in rats by high doses of vitamin E
2. Large doses of vitamin E over at least 3 months can increase peripheral blood circulation and increase walking capacity in the elderly
3. There is presently insufficient evidence that supplemental vitamin E can prevent disorders including ulcers, cancer and heart disease
Animal studies indicate vitamin E can prevent or hinder harmful effects of smog, cigarette smoke, and xenobiotics

VIII. Vitamin E Toxicity

Vitamin E appears to be one of the least toxic of the vitamins
1. 400-800 mg of a-tocopherol equivalent have been taken for years without apparent harm
2. Occasional symptoms reported at 800 mg to 3.2 g
  1. Muscle weakness, fatigue
  2. Double vision
  3. Gastrointestinal distress, nausea, diarrhea, flatulence

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Vitamin E (tocopherols) formula C₂₉H₅₀O₂

Vitamin E (tocopherols) — C₂₉H₅₀O₂

A fat-soluble antioxidant that sits in cell membranes and helps stop fat from going rancid inside the body. Alpha-tocopherol is the form humans use most. Food oils and a mixed diet matter more than one giant pill.

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Vitamin A	Vitamin B1 (Thiamin)	Vitamin B2 (Riboflavin)	Vitamin B3 (Niacin)
Vitamin B5 (Pantothenic Acid)	Vitamin B6	Vitamin B12	Vitamin C
Vitamin D	Vitamin E	Vitamin K	Biotin
Folic Acid

Calcium	Magnesium	Phosphorus	Sodium, Potassium, Chloride
Sulfur (Sulfer)

Boron	Chromium	Cobalt	Copper
Fluorine	Iodine	Iron	Manganese
Molybdenum	Nickel (Nickle)	Selenium	Silicon
Tin	Vanadium	Zinc	Ultra Trace

Aluminum	Arsenic	Cadmium	Lead
Mercury

What the science says (1990–2026): Vitamin E

Vitamin E

Vitamins, Major Elements, Trace Elements, Toxic Elements

Vitamins

Major Elements

Trace Elements

Toxic Elements

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