Forum Navigation
You need to log in to create posts and topics.

Vitamin E protection (tocopherols, tocotrienols)

To support this work, there are Nutrition Restored evaluated Vitamin E products with affiliate links at the end of this article.

See my other article on how Poison/"Vitamin A" specifically depletes Vitamin E here.

Vitamin E is a complex topic.  Here's what I have to say about it.

To begin, I have multiple studies linked in my Cod liver oil is a poison and the research has always said so article showing how Vitamin E was protective against the purposeful hypervitaminosis A poisoning via cod liver oil in multiple different species of lab animals.

Then, we have some more recent research:

Clinical Pearl: Vitamin E (α-tocopherol), 800 IU daily, may reduce retinoid toxicity

In a study of patients with myelodysplastic syndrome who were treated with high-dose (100 mg/m2) oral 13-cis -retinoic acid daily, the addition of vitamin E (α-tocopherol) prevented retinoid-induced side effects in a high proportion of patients.1 Of 66 patients studied, 45 were treated concomitantly with vitamin E, 800 IU daily. In 100% of patients treated with 13-cis -retinoic acid alone cheilosis developed, compared with 31% treated with a combination of 13-cis -retinoic acid and vitamin E. Hyperkeratosis developed in 100% of patients treated with the drug alone compared with 27% treated with the combination regimen.

EFFICACY OF ORAL VITAMIN E IN DECREASING MUCOCUTANEOUS SIDE EFFECT OF ISOTRITINOIN

Isotretinoin represents the treatment that has been shown to induce long-term remissions and even to “cure” acne. A lot of side effects can result from its use especially mucocutaneous, which may lead to discontinuation of the drug. Some reports recommend the addition of vitamin E in oral dose to lower the severity of mucocutaneous side effects of isotretinoin. Study was conducted to investigate the efficacy of oral vitamin E on mucocutaneous side effect of isotretinoin. Forty acne patients receiving isotretinoin 1mg/kg/day were divided in to two groups; with and without 800IU of oral vitamin E and follow up for mucocutaneous side effect over four months duration. In conclusion, this study revealed that despite the administration of vitamin E significantly decrease chelitis which is the most common annoying isotretinoin mucocutaneous side effect, additional future studies are needed to confirm our results.
[...]
Some reports suggest that using retinoids with vitamin E leads to improvements of some side effects due to isotretinoin because vitamin E levels decreased during isotretinoin treatment and some of the side effects due to isotretinoin treatment might be related to this, and supplementation vitamin E may be useful during isotretinoin treatment [19].

Vitamin A toxicity and vitamin E deficiency in a rabbit colony.

Vitamin A toxicosis and vitamin E deficiency was diagnosed in a commercial rabbit-breeding colony and was associated with reproductive abnormalities, abortions, and poor survivability of kits in the breeding colony. Paresis and muscular dystrophy were noted in juvenile rabbits. Another group of New Zealand White rabbits from the same commercial colony was used to assess the effect of vitamin E-based therapy on clinical signs, reproduction, and vitamin A and E serum and liver levels. Blood samples were taken before and after dietary changes and vitamin E therapy. Serum vitamin E remained low after feeding a diet containing the recommended levels of vitamin E. Administration of vitamin E for 2 weeks lowered the serum vitamin A levels and increased the vitamin E serum and liver levels. In conclusion, vitamin E therapy appears to be an effective treatment for hypervitaminosis A.

Important to note about the above study..."feeding a diet containing the recommended levels of Vitamin E"--think here of the RDA "minimal" levels for humans that 93% of people aren't even getting to daily!!!--resulted in continuing low levels of serum Vitamin E (ie. it wasn't enough to undo the Poison/"Vitamin A" damage).  2 weeks of "Vitamin E therapy" lowered Poison/"Vitamin A" levels AND also raised Vitamin E levels in the blood and liver.   This is exactly why I no longer believe that food Vitamin E alone is sufficient during the Poison/"Vitamin A" Detox Program period.

Inhibition of vitamin A synthesis by excess [alpha]-tocopherol in young rats [PDF attached]

Growth
The daily consumption of excessive amounts of aT [alpha-tocopherol] did not have any adverse effect on the growth rate of rats over feeding periods up to 56 days.

Hepatic Retinol
Hepatic deposition of ROL was almost completely abolished when rats received daily supplements of 50 mg aT together with beta-carotene as their sole source of vitamin A (Experiments 1A and 3A). The feeding period was extended from 28 to 56 days, yet the inhibitory effect of excess aT on hepatic ROL deposition persisted (Experiment 6).

Influence of excess vitamin E on vitamin A toxicity in rats.

Male Holtzman rats (78 g) were fed semipurified 16% protein diets for 8 weeks using a food grade soy protein concentrate as the protein source. The basal diet (A) contained added DL-methionine (0.26%) and adequate amounts of vitamins A (14,535 IU/kg as retinyl acetate) and E (60 IU/kg as DL-alpha-tocopheryl acetate) and all other required nutrients. Experimental diets included: (B) basal plus 600 IU of vitamin E/kg; (C) basal plus 6,000 IU of vitamin E/kg; (D) basal plus 2.9 X 10(6) IU of vitamin A/kg; (E) basal plus 2.9 X 10(6) IU of vitamin A plus 600 IU of vitamin E/kg; and (F) basal plus 2.9 X 10(6) IU of vitamin A plus 6,000 IU of vitamin E/kg. Both vitamin A and vitamin E had a significant (P less than 0.05) effect on growth. There was an increase in growth with vitamin E intake and a decrease in growth with vitamin A intake. The net result of these two effects was that the groups fed both vitamins tended to be quite close in mean values to the group fed only the basal diet. Vitamin A significantly (P less than 0.05) increased relative weights of spleen and testes; vitamin E reduced that effect. Vitamin E also significantly (P les s than 0.05) reduced relative adrenal weight whereas vitamin A significantly increased it. The two effects tend to cancel each other in the sense that the group fed both vitamins had an average relative adrenal weight quite close to that of the group fed only the basal diet. However, vitamin A still had an effect even when 6,000 IU of vitamin E was fed. The interaction effect of the two vitamins was significant (P less than 0.05) for plasma total protein and liver vitamin A. There was an increase in liver vitamin A with increasing levels of vitamin E in the diet. Blood urea nitrogen and plasma cholesterol were unchanged. A significant interaction of vitamins A and E was found to effect plasma total protein, liver vitamin A, and relative weight of spleen and testes.

Excessive Dietary Vitamin E: Its Alleviation of Hypervitaminosis A and Lack of Toxicity [abstract #1]

Strangely, the paper linked above has two different abstracts that can be found.  They're both useful, so I'm linking both.

Abstract
Cockerels from 1 day of age were given for 32 days vitamin A, E or both in about 1000 times the amount usually considered best. For 2 groups the extra vitamin A was removed after 18 days and one of those groups then got extra vitamin E. Mortality was high with excess vitamin A. Simultaneous intake of large amounts of vitamin E completely prevented that effect. Excess vitamin E alone had no effect on mortality. Excess vitamin A depressed growth and this was largely overcome by addition of vitamin E throughout the feeding period; recovery from depression of growth after the removal of vitamin A at 18 days was not affected by excess vitamin E. Excess vitamin E alone did not affect growth. The livers of chickens given more vitamin A were small and those given more vitamin E were larger. Those of the chickens on the basal diet or with both vitamins were similar. It is suggested that the protective action of vitamin E is due to its antioxidant properties and that vitamin A causes oxidative destruction of tissues.

Excessive Dietary Vitamin E: Its Alleviation of Hypervitaminosis A and Lack of Toxicity [abstract #2]

HYPERVITAMINOSIS A has been reported in several species particularly in domestic pets (Seawright et al., 1965) which were fed large amounts of liver, and in humans (Persson et al., 1965) due to therapeutic overdoses of vitamin A. High levels of this vitamin were also shown to have a detrimental effect on calcification in cows (Manston, 1966). On the other hand, comparable levels of vitamin A have been used experimentally in combination with massive doses of vitamin D3 to treat milk fever in lactating cows (Payne and Manston, 1967) without toxic effects of either vitamin. This antagonistic action of vitamins A and D on the toxicity of each other has been studied in chicks by Taylor et al.(1968). The present report indicates that the toxicity due to excessive vitamin A can be counteracted by large doses of vitamin E.

Vitamin E prevents side effects of high doses of vitamin A in chicks.

In good news, there seems to be one country in particular that is "getting it" in regards to the Poison/"Vitamin A" toxicity problem.  That country is Finland.  They suggest that pregnant and nursing women, along with children under 1 year old, completely avoid eating liver-related products due to its Poison/"Vitamin A" content.  There are also the studies below from Finland--in both men and women--showing that one's Vitamin E status seems to highly correlate with one's risk of cancer:

Vitamin A, vitamin E and selenium status in an aged Finnish male population.

The association between serum alpha-tocopherol levels and the subsequent incidence of cancer was investigated in a longitudinal study of 21,172 men initially aged 15-99 years in six geographic areas in Finland. The baseline examination was conducted in 1968-1972, and during the follow-up of 6-10 years, 453 cancers were diagnosed. The serum alpha-tocopherol levels were measured from stored serum samples from these men and from 841 male controls, matched for municipality and age, who did not develop cancer during the follow-up. The mean levels of serum alpha-tocopherol among the cancer cases and controls were 8.02 and 8.28 mg/liter, respectively. A high serum alpha-tocopherol level was associated with a reduced risk of cancer. The relative risk of cancer in persons in the two highest (threshold 8.70 mg/liter) quintiles of serum alpha-tocopherol was 0.64 (95 per cent confidence interval = 0.49-0.85) in comparison with those in the three lowest quintiles. The association was strongest for the combined group of cancers unrelated to smoking and varied between subgroups of the study population as well as between different cancers. The association persisted when adjusted for serum cholesterol, serum vitamin A, serum selenium, and various confounding factors. It also persisted when subjects with possible signs of cancer at the time when the blood samples were drawn or with cancers diagnosed during the first two years of follow-up were excluded. These findings agree with the hypothesis that high vitamin E intake protects against cancer.

Serum vitamin E level and risk of female cancers.

A sample of 15,093 women, aged 15-99 and initially free from cancer, participated in the Finnish Social Insurance Institution's Mobile Clinic Health Survey in 1968-71. A record linkage to the Cancer Registry revealed that during a mean follow-up of eight years cancer was diagnosed in 313 women. Serum alpha-tocopherol levels were measured from stored samples (at -20 C) of the cancer patients and of 578 controls, matched for municipality and age. An inverse relation was observed between alpha-tocopherol level and risk of cancer, even if the cancers in the first two years of follow-up were excluded. Women in the lowest quintile for alpha-tocopherol levels compared to those with higher values had a 1.6-fold (95% confidence interval: 1.1-2.5) risk of cancer as adjusted for possible confounding effects of several other factors. A low level of alpha-tocopherol in general strongly predicted epithelial cancers while it carried an only slightly elevated risk of cancers in reproductive organs exposed to oestrogens. The results suggest that a low vitamin E intake is a risk factor for cancer in many, but not all, organs. The expression of its protective effect may depend on the primary causes, which vary between different cancers.

The total number of men and women in the above studies is over 36,000 people.  The one in men says more Vitamin E = less cancer, the one in women says less Vitamin E = more cancer.  Poh-taY-toh, po-taH-toh, do you see?

Knowing what we know now, how can we address the bullet point issues I mentioned at the start of this article?

  • Getting enough Vitamin E daily to protect against Poison/"Vitamin A" toxicity and/or detox would be the best start.
    • The highest Vitamin E foods are listed here.  Getting to the RDA will prove difficult for many with foods only (apparently for 93% of Americans this is true!), particularly when limiting the list to low-carotenoid foods.  Note that the RDA is sort of "the bare minimum", and that the last study I linked above mentioned "large doses", so doing the bare minimum is probably only going to give minimal help at best.  The RDA in the
  • Using a moderate dose, natural-source, non-GMO, minimal-carotenoid-content, mixed-tocopherol supplement is likely to be beneficial.
  • If it were me, I would make the upper limit of Vitamin E supplementation at 400 IU of d-alpha-tocopherol from a mixed tocopherol supplement daily.
  • Avoid all ACETATE forms of Vitamin E in supplements and fortified foods (avoid fortified foods in general!)
  • Do not take supplements (or multis) that only contain d-alpha-tocopherol, make sure the other three tocopherols (beta, gamma, delta) are in there too!
  • To avoid high-carotenoid (plant Poison/"Vitamin A") Vitamin E supplements, and also high-arsenic ones as well, do the following:
    • Avoid Vitamin E supplements derived from red palm oil or annatto.
    • Avoid Vitamin E supplements that are a darker brown or reddish color, this indicates lots of carotenoids.
    • Brown rice (and rice bran, which is the "brown" part) is known to be high in arsenic, so don't buy Vitamin E supplements derived from it either.
    • If you buy a Vitamin E supplement that does contains tocotrienols, make sure to double-check it for the above things.

Are you confused enough yet?  I'll simplify it for you.  If I were going to use a Vitamin E supplement and wanted to support this work at the same time, I might use one of the following links:

  1. Wellevate (helps this project the most): Contact Us to get your personal store invitation.
  2. Vitacost option: NOW Natural E-400 with Mixed Tocopherols, 250 softgels
  3. Swanson option:  Swanson Vitamin E Mixed Tocopherols 400 IU, 250 softgels
  4. iHerb option:  NOW Natural E-400 with Mixed Tocopherols, 250 softgels
  5. Amazon option: NOW Natural E-400 with Mixed Tocopherols, 250 softgels

So there you go.

Uploaded files:
  • You need to login to have access to uploads.
Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
Interested in my comprehensive Poison/"Vitamin A" Detox program? Contact Us
Want to work directly with me? I work with US and International clients! Contact my office
Enjoy seeing this work? Want to see more of it? Donations gratefully accepted! Click Here
If you order from iHerb, use my affiliate coupon code NCJ477 to get 5% Off!
If you order from Amazon, here is the Nutrition Restored Amazon Product List.
FaceBook Notes (aka my "blogging" for a long time)
My YouTube Channel
The goal is to eventually move everything to this website, as social media is without a doubt a great poison to humanity.
Medical Disclaimer