What we’ll do here is cover some basic information about vitamin E as relates to plant-based eating.
First, I’ll answer some common questions for those of you who are in a rush:
- Is vitamin E vegan? Yes, unlike vitamin D (check out the article here), vitamin E is found almost exclusively in plant foods. Additionally, both synthetic forms (vitamin E acetate and succinate) are made without the use of animal products and are thus considered vegan.60
- What are some vegan sources of vitamin E? Common vegan sources of vitamin E include sunflower seeds, almonds, plant oils (especially wheat bran oil), hazelnuts, and peanuts/peanut butter. To a lesser degree, certain fruits and vegetables like kiwifruit, spinach, and broccoli also contain vitamin E.1
- Are vegans commonly deficient in vitamin E? No, not characteristically. According to NIH, the only at-risk groups for vitamin E deficiency include premature infants and people with fat malabsorptive disorders.1
- Is vegan vitamin E effective? Yes, vegan vitamin E is effective because all forms of the vitamin are considered vegan. It’s the configuration of the vitamin that determines how effective it will be. As you’ll see, it’s the natural RRR α-tocopherol that has the most vitamin activity in humans.1
- Is Jason Vitamin E Oil vegan? Yes, Jason Vitamin E Oil is vegan. Again, all vitamin E is vegan. According to the label, the ingredients include tocopheryl acetate (synthetic vitamin E) suspended in various plant oils including sunflower seed oil, safflower oil, rice bran oil, avocado oil, sweet almond oil, apricot kernel oil, and wheat germ oil.2
What we’ll do next is take a closer look at the sources of vitamin E as well as some other basic info.
Overview and Functions
As discussed with vitamin B6, many vitamins exist as “vitamers.” When a vitamin is said to occur as vitamers, it simply means that a handful of different but structurally similar compounds show vitamin activity to one degree or another in different organisms.
As you’ll see, in humans only one of the naturally occurring vitamin E molecules—RRR α-tocopherol—exerts essential vitamin E activity in humans. For our purposes, we needn’t get into the chemistry of what R and S mean. Just know that they’re used to denote different stereoisomers—or configurations of a given molecule.
In food, vitamin E exists as eight different RRR versions divided into two classes:3
- The tocopherols—these have saturated side chains with 16 carbons. They’re designated as α, β, γ, and δ.
- Tocotrienols aka trienols (I guess all the good names were taken). The side chain on these is unsaturated with 16 carbons. They’re also designated from α to δ.
These two classes differ in both the number and location of the methyl groups on the ring at the head of the molecule. Unlike some vitamins that exist as isomers, these eight compounds are not interchangeable—the body can’t interconvert them.
Then you have the synthetic forms of the vitamin. The synthetic (ester) forms of the vitamin include all-rac (all racemic) α-tocopheryl acetate and α-tocopheryl succinate. These are used in vitamin supplements and foods. They also come in eight stereoisomers.
Though less potent, the synthetic forms have vitamin E activity in humans and can be used to meet vitamin E needs.
If it’s confusing, don’t worry because I cleaned it up with the chart below. I bring all of this up because certain versions of the vitamin are less metabolically active than others.4
*When these are present in a supplement the label reads mixed tocopherols.
Vitamin E serves as an antioxidant and is involved in cell signaling in the area of gene expression among others.
Vitamin E serves its main function as an antioxidant where it maintains the integrity of our cell membranes by preventing peroxidation of unsaturated fatty acids (UFAs) in the membrane phospholipids.
Cell membranes that are especially susceptible to oxidation include:
- Brain cell membranes
- Red blood cells (RBCs)
- Lung cell membranes
RBC membranes are very vulnerable to oxidation due to their high polyunsaturated fatty acid (PUFA) content and exposure to high levels of oxygen.
Like carotenoids covered in the vitamin A guide, vitamin E can quench both free radicals (in a process known as chain breaking or free radical termination) and singlet molecular oxygen.
Quenching of Singlet Molecular Oxygen
“Quenching” is the process by which excited molecules or atoms are inactivated. Oxygen in the ground state has an energy level much lower than oxygen in the singlet form. Thus, singlet molecular oxygen is much more reactive.
Ways in which singlet molecular oxygen is generated includes:
- Lipid peroxidation of membranes (where vitamin E and the carotenoids come in)
- Photochemical reactions (energy transfer from light)
- The oxidative or respiratory burst that occurs in some phagocytic cells like neutrophils.
- Redox reactions with organic molecules such as DNA, proteins, and lipids which can destroy molecular components of cells.
The carotenoids are actually much more powerful in preventing lipid peroxidation, but vitamin E is of more physiological significance as it’s present in much higher amounts in the body.5
Earlier we went over how α-tocopherol is the only of the eight naturally occurring vitamin E vitamers that fulfills essential vitamin E functions. That’s in part because not all vitamin E is created equal when it comes to the quenching of singlet molecular oxygen.
The ability of a given form of vitamin E to quench singlet oxygen is related to the head of the molecule—the free hydroxyl group at the 6 position of vitamin E’s chromane ring. Of the eight vitamers, the α-tocopherol was found to the most effective followed by β-, γ-, and δ-tocopherol.5
Quenching of Free Radicals
Like with singlet molecular oxygen, not all forms of vitamin E are equally effective here. The free hydroxyl group of α-tocopherol makes it the most effective in free radical termination, followed by the others (β-, γ-, and δ-tocopherol).
The hydroxyl group donates hydrogen ions to free radicals breaking the chain of oxidation. Free radicals generated in a number of ways (e.g. UV light or enzymatic reactions) can start a series of damaging reactions that can be nipped in the bud by vitamin E. The chain-like reactions take place in three phases: initiation, propagation, and termination.
We won’t go into detail here, but free radicals run around swiping electrons from their environment, usually from organic molecules like lipids. If the molecule is a membrane lipid (PUFA), then the membrane is damaged, and its function diminished. After donating a hydrogen, vitamin E gets oxidized and is later regenerated by compounds like vitamin C, or reacts with other molecules to become stable.
Vitamin E Intake and Cancer
Cancer development is thought to involve three phases. The first phase is the initiation phase wherein it’s thought that free radical-induced damage may trigger cancer by activating a few processes including:6
- Signaling pathways involved in cancer development
- Expression of genes involved in cancer pathophysiology
- Altered cell growth/differentiation
- Changes in enzyme activity
- The production of toxic compounds
To the extent that vitamin E may help prevent the initiation and progression of cancer, it likely doesn’t do it alone. Studies investigating the high intakes of dietary and supplemental vitamin E on cancer risk have found no association.7-16
We’ve talked before about nutrient synergy—the idea that plant compounds often work together synergistically in a way that likely accounts for the health benefits associated with the consumption of whole plant foods.
There may be a relationship between the consumption of vitamin E-containing foods and cancer, but thus far most of the evidence suggests little to no association.
Vitamin E Intake and Heart Disease
Also outlined in the vitamin A article, it’s thought that antioxidants may help prevent heart disease by preventing the oxidation of LDL particles. When LDL cholesterol is oxidized, lipid-packed “foam cells” get lodged in the blood vessel walls eventually forming an atheroma in a process involving several steps.
First, monocytes adhere to the lining of the blood vessels where they migrate into the innermost layers of the vessel walls, and gobble up oxidized LDL cholesterol, resulting in foam cells, fatty streaks, and plaque.
Vitamin E helps prevent the oxidation of LDL, thus helping stave off artery occlusion and blood clot formation.4
Vitamin E Intake and Eye Health
Yet another similarity to vitamin A. It’s thought that vitamin E may help in the treatment and prevention of age-related macular degeneration (AMD) and cataracts.
Many studies have found low intakes of antioxidants (especially vitamins E and C), to be associated with AMD and cataract development. It makes sense. After all, it’s thought that free radical-induced damage likely contributes to the development of these two conditions.
So far the only support for this idea comes from prospective cohort and epidemiological studies.17-22 Unfortunately, several other studies failed to show a significant effect.23-25
Vitamin E Intake and Other Conditions
Other diseases with potential vitamin E significance include:
- Diseases characterized by lipid peroxidation (e.g. diabetes and iron overload).
- Diabetes mellitus—improved cell membrane structure may improve glucose uptake, lowering insulin resistance.
- Alzheimer’s and other neurodegenerative diseases—the protein aggregates that accumulate in such diseases are thought to potentially be caused by oxidative stress.
As for neurodegenerative diseases, few studies have shown any benefit to be conferred by high vitamin E intakes or supplementation.26-28
As such, evidence is lacking for the use of the vitamin in helping treat or prevent Alzheimer’s and other neurodegenerative diseases.29,30
Cell Signaling, Gene Expression, and Other Roles
Vitamin E also functions in cell signaling where it interacts with transcription factors (TFs) and cell receptors. In doing so, it affects enzyme activity and gene expression among other things.
These functions involve:
- Inhibition of protein kinase C.31
- Transcriptional regulation of antioxidant defense, cell cycle, and steroid synthesis (e.g. cholesterol) among other processes.32
- Interaction with a certain type of RNA known as micro (mi)RNAs where it inhibits multiple genes.32,33
- Aside from α-tocopherol, tocotrienols have significant roles in the area of gene expression. For example, they suppress the activity of (HMG)-CoA reductase in cholesterol synthesis reducing plasma cholesterol concentrations. They’re also involved in cell signaling pathways including those involving insulin and estrogen receptors, and anti-inflammatory activities.34-36
Vitamin E is one of the most vegan-friendly nutrients. It’s found primarily in plant foods, especially oils. In fact, of the many food sources listed on NIH, every single one is in the plant kingdom.
- Plant oils. For example, wheat germ and sunflower oils contain 20.2 mg /Tbsp. and 5.5 mg /Tbsp., respectively. For wheat germ oil, that comes to 101% DV. These two are particularly rich in α-tocopherol, the metabolically active form of vitamin E. Soybean and corn oils are high in vitamin E but contain more γ-tocopherol and less α-tocopherol.37-39
- Nuts and nut
butters. For example, almonds, peanuts, and cashews provide 7.0 mg/oz, 2.2 mg/oz, and 0.3 mg/oz of α-tocopherol, respectively.40
- Certain fruits and veggies. Per ½ cup, spinach, collard greens, and broccoli contain 1.2 mg, 1.9 mg, and 0.8 mg of α-tocopherol, respectively.40
Most of the foods listed in this article are good sources of α-tocopherol because that’s the form most useful for vitamin E functions in the body. As we saw with gene expression, tocotrienols do have important roles to play as well.
This form of the vitamin tend to be present in food in very small amounts.
Some sources include:
- Fruits and veggies—while the green, chloroplast-containing portion of plants such as the leaves mostly contain α-tocopherol, other parts of the plant provide δ-, γ-, and β-tocopherols.40
- Cereal grains—especially barley, rice, and oats (though it can be removed in the milling process).
- Plant oils—palm oil is one of the richest sources with 70% of the vitamin E as tocotrienols. It also happens to be primarily composed of saturated fats.
Other than that, most sources of tocotrienols tend to be animal products.
Best Practices to Avoid Nutrient Loss/Deficiency
As with other fat-soluble vitamins, vitamin E is susceptible to destruction throughout food processing, preparation and storage process.
In grains, vitamin E is most concentrated in the wheat germ which is removed during processing. This significantly reduces the vitamin E content of grain products. For example, one cup of raisin bran boasts a mere 0.4 mg (2% DV) of vitamin E.41
Tocopherol, being the antioxidant form of vitamin E is oxidized over time when exposed to air, heat, and light all of which increase destruction of the vitamin.
Vitamin E is widely distributed in nuts. Unfortunately, the roasting of nuts like peanuts and almonds reduces their vitamin E content—though it also makes the cell structure easily broken increasing the bioavailability of many nutrients.
All vitamin E supplements are vegan, including natural α-tocopherol, α-tocopheryl acetate, α-tocopheryl succinate, and mixed tocopherols. If you’re looking for mixed tocopherols or a specific isomer, the form of the vitamin should be listed on the supplement label. So you know, the α-tocopherol is commonly labeled dl-alpha-tocopherol
However, since vitamin E is delivered in oil, you’ll just need to make sure the capsules are vegan-friendly as some capsules are made of gelatin. You’ll want to use vegetable capsules which are made of hypromellose (a cellulose-like polymer).
Food Versus Supplements
As discussed earlier, it seems logical that vitamin E intake may confer protection against cancer and other diseases where oxidative damage is implicated in the etiology. Unfortunately, most recent RCTs have failed to show beneficial effects of vitamin E supplementation in reducing heart disease risk.42,43,7,44-49,8
For those already having heart disease, only a few studies have found supplementation with vitamin E to slow progression of atherosclerosis, reduce the risk of embolisms, or decrease CVD mortality.8,50,51
Results from two studies actually found vitamin E supplementation to potentially increase mortality.52,53
In one meta-analysis of 19 RCTs looking at vitamin E supplementation outcomes, a dose-response relationship was found between all-cause mortality and daily supplementation with 400 IU vitamin E for one year.54
Another study randomized 423 postmenopausal women with heart disease to two groups: one receiving 500 mg of vitamin C plus 400 IU vitamin E twice daily, and the other receiving a placebo. It found the intervention group to have a significantly higher total mortality and CVD mortality compared to control.55
One randomized trial assigned 14,000 male physicians 50 years and older to either daily supplementation of 400 IU of synthetic α-tocopherol plus 500 mg vitamin C, or to a placebo group. While supplementation had no effect on the incidence of heart attack, stroke incidence significantly increased in the intervention group.46
Select Vitamin E Sources
Recommended Daily Allowance (Needs)
The adult RDA for vitamin E is 15 mg per day of α-tocopherol for both men and women.4
Needs go up a bit during lactation increasing to 19 mg or 28.4 IU per day.
Those who smoke may benefit from additional vitamin E, however, no specific recommendations have been set for this population.1,56
The Food and Nutrition Board (FNB) recommends that in meeting your needs, you limit vitamin E to the naturally occurring RRR α-tocopherol and to three of the synthetic forms (highlighted in the chart).4
The synthetic forms are less potent, but you don’t need to worry with any conversions, as the food and supplement labels crunch all the numbers for you in terms of what %DV the dose counts for. Which is all that matters.
They’ll be doing away with IU on supplement labels soon anyway, and will just list mg and %DV.57,58
Plasma concentrations of α-tocopherol of less than 5 μg/mL suggest deficiency. Most notably, vitamin E deficiency is associated with hemolytic anemia—the form of anemia in which RBCs are destroyed at a faster rate than they’re made.
Other symptoms of vitamin E deficiency include:59
- Myopathy (skeletal muscle pain)
- Muscle weakness
- Accumulation of ceroid pigments
- Degenerative neurological problems: ataxia, peripheral neuropathy, loss of coordination, and loss of vibratory sense.
Like any vitamin, some folks have less than adequate intake of vitamin E. However, deficiency of the vitamin in humans is rare. Only a handful of population groups are at risk: premature infants and folks with fat malabsorption disorders.1
Premature infants often have impaired fat utilization due to prematurity. Certain conditions like cystic fibrosis are characterized by a deficiency of pancreatic lipase—the enzyme needed to break fat down in order to absorb it.
Disorders of the hepatobiliary system (e.g. chronic cholestasis) are characterized by a decrease in bile production—bile is needed to emulsify fat in order for it to be digested and absorbed. There are other obscure conditions you probably haven’t heard of that can lead to vitamin E deficiency, but you get the idea.
The Vegan Diet and Vitamin E Status
Not much to say here thankfully. Vitamin E is ubiquitous in the plant kingdom. So much so that even omnivores with poor veggie intakes tend to have adequate vitamin E status. If you’re a high-carb vegan (as many raw vegans are) who tends to avoid nuts, seeds, and plant oils you may have a hard time getting enough of the vitamin. But even raw vegans tend to include some amount of nuts and seeds in their diet. So, overall this isn’t a huge area of concern for vegans.
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- U.S. Food and Drug Administration. Food Labeling: Revision of the Nutrition and Supplement Facts Labels and Serving Sizes of Foods That Can Reasonably Be Consumed at One Eating Occasion; Dual-Column Labeling; Updating, Modifying, and Establishing Certain Reference Amounts Customarily Consumed; Serving Size for Breath Mints; and Technical Amendments; Proposed Extension of Compliance Dates.external link disclaimer 2017.
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