TocoVit - Liquid Vitamin E From Wheat Germ Oil

[inurendotoxin]

I tried Tocovit for my mild gyno. There is a definite shrinking of glandular tissue and nipple size. I'll continue taking it to see how this progresses, but it's pretty crazy. I've been taking vitamin E for several years and have never seen an effect. Nor have I seen an effect from any supplement, really. I also took a few drops of magnoil, so I suppose I should try it on it's own next. Will report back in a few weeks with more info... pretty interesting though!

This is interesting. Any update from the Tocovit (vs Magnoil)-only approach?

 

[hmac]

This is interesting. Any update from the Tocovit (vs Magnoil)-only approach?

I do like the Tocovit, very much. However, the magnoil doesn't agree with me, so I don't use it any more. I haven't noticed an improvement in the gyno from the original decrease in puffiness. It is the only vitamin E which doesn't give me skin irritation when I apply it topically, so that is interesting.

 

[ecstatichamster]

I find that it’s perfectly fine to take vitamin K2 with E. I can tell it is because I take it with a lot of aspirin and it still totally prevents bleeding or bruising even if taken together.

 

[Amazoniac]

For those that use vitamin E..

'Advanced Nutrition and Human Metabolism' (978-1-133-10405-6):

"Because the antioxidant functions of vitamin E in the body are closely tied to those of selenium-dependent glutathione peroxidase (an enzyme that converts lipid peroxides into lipid alcohols), an interrelationship exists between vitamin E and selenium. The actions of both nutrients are complementary, and higher concentrations of one nutrient can reduce the effects of lower concentrations of the other nutrient."

 

[whodathunkit]

Would you be kind enough to let me know if you experience the same effects on the 'new' formulation of Tocovit since Haidut purified into just the mixed tocopherols/policosanol? I’m having slightly different effects but I’m very keen to see if this new formulation induces menstruarion shortly after a large dose, as that would be a reliable marker of estrogen reduction. Thanks @whodathunkit.

I'll start my new bottle for you today .It's a couple weeks old .I don't really use it to regulate my cycle but it will bring it o n if I get tired of effing around with it (And I am currently quite tired lol)

 

[Jackrabbit]

I’m not sure if this information was already posted because I don’t have time or patience to read through 22 pages of this thread but I was listening to a kmud interview with Dr. Peat yesterday where he discusses vitamin e dosage for fertility in women over 40 and he said it was at least 400 iu, but could be more depending on PUFA intake. I decided to settle on 12 drops of tocovit and have already noticed a more restful sleep. The first couple of days of increased dose I had somewhat painful diarrhea but it wasn’t long lasting and I felt that it was detoxing. Thanks, haidut, for this supplement. Other e supplements have given me a lot of gas, so it’s great to have one that doesn’t cause that.

 

[Amazoniac]

I was going to post this elsewhere, but it's probably more useful here.

These days, the only other viable option to using a soap with an unwanted addition of (natural) vitamin E is to prepare my own, which I'm not willing to for now.

I've been experiencing detrimental effects that are likely from vitamin E, the impairment is systemic. I don't seem to have any problems with ingested vitamin E, but things are different with topical. Random dosing might play a rôle, I haven't checked with the company yet, but the amounts are probably not extreme. There is no irritation at all, so this can be ruled out. Some time ago I reacted to TocoVit but that was when it wasn't refined, never had a problem in this regard after the modification.

Not much success when searching for reports on odd effects from its topical use other than what has already been posted. No satisfactory results for difference in tissue distribution depending on the route either, but this must also be involved.

In terms of interactions, I have the impression that it increases my need for vit C dramatically, which is already higher than average. The simplest explanation would be due to recycling of vitamin E. But there might be more to the story..

- Handbook Of Vitamins, Minerals And Hormones - Roman J. Kutsky

Here's what the author has collected from multiple sources:

Antagonists (1, 7, 14, 16, 26, 34)
a-Tocopherol quinone, oxidants, codliver oil, thyroxine, [Fe]3+

Synergists (1, 7, 14, 16, 26, 34)
Vitamins A, 85, B12, C, K, folic acid, estradiol, testosterone, STH, [SeO3]2-, [Zn]2+

Half-life (8, 9, 29, 31, 32, 34)
Approx. 2 weeks

Target Tissues (14, 16, 29, 31, 32, 34)
Kidneys, genital organs, muscles, liver, lungs, bone marrow, adrenals, pituitary

The numbers are the references located at the end of each chapter.

[34] Book Series: Vitamins And Hormones (Vol 5)​

- Nutritional Toxicology (Vol 1 out of 3) (0-12-332601-X) - John Hathcock

Spoiler: Mild crash

These are good books as well.

- Fe2+ Catalyzes Vitamin E-Induced Fragmentation of Hydroperoxy and Hydroxy Endoperoxides That Generates γ-Hydroxy Alkenals

- Vitamin E decreases bone mass by stimulating osteoclast fusion

In my experience 'sunlighter + vit K2 as mk-7 + vitamin E' is a synergistic program to deplete vitamin C.

 

[Amazoniac]

- Coenzyme Q and Vitamin E Interactions
- Dietary Coenzyme Q10 and Vitamin E Alter the Status of These Compounds in Rat Tissues and Mitochondria

 

[RayPeatFan777]

I’m not sure if this information was already posted because I don’t have time or patience to read through 22 pages of this thread but I was listening to a kmud interview with Dr. Peat yesterday where he discusses vitamin e dosage for fertility in women over 40 and he said it was at least 400 iu, but could be more depending on PUFA intake. I decided to settle on 12 drops of tocovit and have already noticed a more restful sleep. The first couple of days of increased dose I had somewhat painful diarrhea but it wasn’t long lasting and I felt that it was detoxing. Thanks, haidut, for this supplement. Other e supplements have given me a lot of gas, so it’s great to have one that doesn’t cause that.

Did you take it orally?

 

[Jackrabbit]

Did you take it orally?

I wasn’t before but I’ve started to do a combo of oral and rubbing into the gums. Yesterday I managed to stop a migraine that was starting with a 14 drop dose

 

[Braveheart]

For those that use vitamin E..

'Advanced Nutrition and Human Metabolism' (978-1-133-10405-6):

"Because the antioxidant functions of vitamin E in the body are closely tied to those of selenium-dependent glutathione peroxidase (an enzyme that converts lipid peroxides into lipid alcohols), an interrelationship exists between vitamin E and selenium. The actions of both nutrients are complementary, and higher concentrations of one nutrient can reduce the effects of lower concentrations of the other nutrient."

So what are these higher concentrations?

 

[Amazoniac]

Still on a quest to find out what's the deal with topical vitamin E, it's brutal and puzzling.

- Modern nutrition in wealth and disease (978-1-60547-461-8)

"Deuterated a-tocopherol has been used to assess the kinetics and distribution of a-tocopherol into various tissues in rats (83), guinea pigs (84), and humans (85). From these studies, it is apparent that groups of tissues, such as erythrocytes, liver, and spleen, are in rapid equilibrium with the plasma a-tocopherol pool and readily replace “old” with “new” a-tocopherol (86). Other tissues such as heart, muscle, and spinal cord have slower a-tocopherol turnover rates. Brain shows the slowest a-tocopherol turnover rate, perhaps because it expresses a-TTP (65, 87). In humans, the peripheral nerves (6) are the most susceptible tissues to a-tocopherol deficiency (88)."​

- Advanced Nutrition and Human Metabolism (978-1-133-10405-6)

"The half-life of RRR α-tocopherol in the plasma is about 48 hours, whereas the stereoisomer SRR α-tocopherol has a half-life of about 13 to 15 hours [4]."

Determination of Phylloquinone and Menaquinones in Food
"Another remarkable difference between K1 and menaquinones was that the former had a disappearance curve with an apparent half-life time of 1.5 h, whereas the long chain menaquinones (not MK-4) had more complex disappearance curves with a very long half-life time."

Kuinone - Liquid Vitamin K2 (MK-4)
"α-TOH, or even α-CEHC, interferes with an intermediate step in the formation of tissue-specific menaquinone-4 from phylloquinone"
​

"Chylomicron remnants deliver vitamin E (absorbed tocopherols and tocotrienols) to the liver. However, only RRR α-tocopherol is incorporated into very-low-density lipoproteins (VLDLs) for resecretion back into the blood and transport to other tissues. It is α-tocopherol transfer protein (αTTP), which is made in the liver (among other tissues), that transfers tocopherol (RRR α-tocopherol preferentially) into VLDLs, which enable distribution of the vitamin to tissues."

"There is no single storage organ for vitamin E. The largest amount (over 90%) of the vitamin is concentrated in an unesterified form in fat droplets in adipose tissue. The concentration of vitamin E in adipose tissue increases linearly with the dosage of vitamin E; however, release of vitamin E from adipose tissue is slow even during periods of low vitamin E intake. Other tissues that take up smaller amounts of vitamin E include the liver, lungs, heart, muscle, adrenal glands, spleen, and brain. The vitamin E concentration in these tissues remains constant or increases only at a slow rate with increased ingestion of the vitamin. Yet, during times in which vitamin E intake is low, the liver and plasma provide a readily available source of the vitamin, in addition to skeletal muscle, which, because of its large mass, contains appreciable amounts."

On excretion
"Hepatic metabolism of vitamin E begins with an ω-hydroxylation reaction, requiring cytochrome P-450, to form hydroxychromanol. Next, a series of reactions analogous to β-oxidation of fatty acids follows to effectively truncate vitamin E’s phytyl side chain. The end products include a group of carboxyethyl hydroxychromans (abbreviated CEHC). Prior to urinary or fecal excretion, these carboxyethyl hydroxychromans are usually conjugated to glucuronic acid or sulfate. Urinary excretory products of the vitamin also include α-tocopheronic acid and α-tocopheronolactone conjugated to either glucuronic acid or sulfate."
​

- Vitamin E - Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids - NCBI Bookshelf

"While the efficiency of vitamin E absorption is low in humans, the precise rate of absorption is not known with certainty. In the early 1970s, vitamin E absorption was estimated to be 51 to 86 percent, measured as fecal radioactivity following ingestion of α-tocopherol (Kelleher and Losowsky, 1970; MacMahon and Neale, 1970). However, when Blomstrand and Forsgren (1968) measured vitamin E absorption in two individuals with gastric carcinoma and lymphatic leukemia, respectively, they found fractional absorption in the lymphatics to be only 21 and 29 percent of label from meals containing α-tocopherol and α-tocopheryl acetate, respectively."

Mechanisms for the prevention of vitamin E excess
"The estimation of the fractional rate of vitamin E absorption varies widely with no consensus among investigators as to whether the percentage is less than 30% or as much as 90%, because the outcomes are highly dependent upon the analytical techniques used and size of the dose (16, 49). There is evidence for a limitation in α-tocopherol absorption, with high doses being absorbed at lower fractional rates (44, 50–53)."

Somewhere between 0 and 100%.
​

Adverse effects
"Uncontrolled studies have reported various other adverse effects associated with excess intake of α-tocopherol. These include fatigue, emotional disturbances, thrombophlebitis, breast soreness, creatinuria, altered serum lipid and lipoprotein levels, gastrointestinal disturbances, and thyroid effects (Anderson and Reid, 1974; Bendich and Machlin, 1988; Machlin, 1989; Tsai et al., 1978). However, none of these reported effects have been consistently observed or shown in controlled trials. Although side effects have been reported with extended intakes of 1,100 to 2,100 mg/day of RRR-α-tocopherol (Kappus and Diplock, 1992), these effects are not severe and subside rapidly upon reducing the dosage or discontinuing the administration of α-tocopherol. The lack of systematic observations of such effects in controlled clinical trails prevents any judgments regarding the risk of such effects in the normal healthy human population."
​

- Bioavailability of vitamin E in humans: An update

- Complexity of vitamin E metabolism
[46] Absorption, Transport and Distribution of Vitamin E


- Metabolism of vitamin E during skin permeation
[6] Dermal penetration and systemic distribution of 14C-labeled vitamin E in human skin grafted athymic nude mice (only abstract available)

"In vivo percutaneous penetration and tissue distribution of 14C-labeled vitamin E applied to human skin grafted onto athymic nude mice were determined. At 1 hr, mouse skin contained the highest level of radioactivity, followed by the muscle, blood, liver, lung, adipose tissue, spleen, kidney, brain, heart, and eyes. A linear increase with time in tissue radioactivity was observed throughout the 24 hr experimental period. At 4 and 24 hrs skin grafts were highly radioactive. At 4 hrs the epidermis and the upper portion of the dermis contained more radioactivity than the remaining portion of the dermis. In contrast, at 24 hrs the highest level of radioactivity was detected in the lower dermis. No radioactivity was detected in expired air while 0.2% of the dose was found in the urine. The data show that vitamin E does penetrate skin and that the dermis acts as a barrier or reservoir for this highly lipophilic compound."​

- Penetration and distribution of α-tocopherol, α- or γ-tocotrienols applied individually onto murine skin


- Mechanisms for the prevention of vitamin E excess


- Inhibition of various glutathione S-transferase isoenzymes by RRR-α-tocopherol

- The Relationship Between Dose of Vitamin E and Suppression of Oxidative Stress in Humans


If someone has a light, do shine.

So what are these higher concentrations?

They didn't specify. I would make sure to not be insufficient on the other and it should be enough to prevent issues.

 

[milk_lover]

Still on a quest to find out what's the deal with topical vitamin E, it's brutal and puzzling.

- Modern nutrition in wealth and disease (978-1-60547-461-8)

"Deuterated a-tocopherol has been used to assess the kinetics and distribution of a-tocopherol into various tissues in rats (83), guinea pigs (84), and humans (85). From these studies, it is apparent that groups of tissues, such as erythrocytes, liver, and spleen, are in rapid equilibrium with the plasma a-tocopherol pool and readily replace “old” with “new” a-tocopherol (86). Other tissues such as heart, muscle, and spinal cord have slower a-tocopherol turnover rates. Brain shows the slowest a-tocopherol turnover rate, perhaps because it expresses a-TTP (65, 87). In humans, the peripheral nerves (6) are the most susceptible tissues to a-tocopherol deficiency (88)."​

- Advanced Nutrition and Human Metabolism (978-1-133-10405-6)

"The half-life of RRR α-tocopherol in the plasma is about 48 hours, whereas the stereoisomer SRR α-tocopherol has a half-life of about 13 to 15 hours [4]."

Determination of Phylloquinone and Menaquinones in Food
"Another remarkable difference between K1 and menaquinones was that the former had a disappearance curve with an apparent half-life time of 1.5 h, whereas the long chain menaquinones (not MK-4) had more complex disappearance curves with a very long half-life time."

Kuinone - Liquid Vitamin K2 (MK-4)
"α-TOH, or even α-CEHC, interferes with an intermediate step in the formation of tissue-specific menaquinone-4 from phylloquinone"
​

"Chylomicron remnants deliver vitamin E (absorbed tocopherols and tocotrienols) to the liver. However, only RRR α-tocopherol is incorporated into very-low-density lipoproteins (VLDLs) for resecretion back into the blood and transport to other tissues. It is α-tocopherol transfer protein (αTTP), which is made in the liver (among other tissues), that transfers tocopherol (RRR α-tocopherol preferentially) into VLDLs, which enable distribution of the vitamin to tissues."

"There is no single storage organ for vitamin E. The largest amount (over 90%) of the vitamin is concentrated in an unesterified form in fat droplets in adipose tissue. The concentration of vitamin E in adipose tissue increases linearly with the dosage of vitamin E; however, release of vitamin E from adipose tissue is slow even during periods of low vitamin E intake. Other tissues that take up smaller amounts of vitamin E include the liver, lungs, heart, muscle, adrenal glands, spleen, and brain. The vitamin E concentration in these tissues remains constant or increases only at a slow rate with increased ingestion of the vitamin. Yet, during times in which vitamin E intake is low, the liver and plasma provide a readily available source of the vitamin, in addition to skeletal muscle, which, because of its large mass, contains appreciable amounts."

On excretion
"Hepatic metabolism of vitamin E begins with an ω-hydroxylation reaction, requiring cytochrome P-450, to form hydroxychromanol. Next, a series of reactions analogous to β-oxidation of fatty acids follows to effectively truncate vitamin E’s phytyl side chain. The end products include a group of carboxyethyl hydroxychromans (abbreviated CEHC). Prior to urinary or fecal excretion, these carboxyethyl hydroxychromans are usually conjugated to glucuronic acid or sulfate. Urinary excretory products of the vitamin also include α-tocopheronic acid and α-tocopheronolactone conjugated to either glucuronic acid or sulfate."​

- Vitamin E - Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids - NCBI Bookshelf

"While the efficiency of vitamin E absorption is low in humans, the precise rate of absorption is not known with certainty. In the early 1970s, vitamin E absorption was estimated to be 51 to 86 percent, measured as fecal radioactivity following ingestion of α-tocopherol (Kelleher and Losowsky, 1970; MacMahon and Neale, 1970). However, when Blomstrand and Forsgren (1968) measured vitamin E absorption in two individuals with gastric carcinoma and lymphatic leukemia, respectively, they found fractional absorption in the lymphatics to be only 21 and 29 percent of label from meals containing α-tocopherol and α-tocopheryl acetate, respectively."

Mechanisms for the prevention of vitamin E excess
"The estimation of the fractional rate of vitamin E absorption varies widely with no consensus among investigators as to whether the percentage is less than 30% or as much as 90%, because the outcomes are highly dependent upon the analytical techniques used and size of the dose (16, 49). There is evidence for a limitation in α-tocopherol absorption, with high doses being absorbed at lower fractional rates (44, 50–53)."

Somewhere between 0 and 100%.
​

Adverse effects
"Uncontrolled studies have reported various other adverse effects associated with excess intake of α-tocopherol. These include fatigue, emotional disturbances, thrombophlebitis, breast soreness, creatinuria, altered serum lipid and lipoprotein levels, gastrointestinal disturbances, and thyroid effects (Anderson and Reid, 1974; Bendich and Machlin, 1988; Machlin, 1989; Tsai et al., 1978). However, none of these reported effects have been consistently observed or shown in controlled trials. Although side effects have been reported with extended intakes of 1,100 to 2,100 mg/day of RRR-α-tocopherol (Kappus and Diplock, 1992), these effects are not severe and subside rapidly upon reducing the dosage or discontinuing the administration of α-tocopherol. The lack of systematic observations of such effects in controlled clinical trails prevents any judgments regarding the risk of such effects in the normal healthy human population."​

- Bioavailability of vitamin E in humans: An update

- Complexity of vitamin E metabolism
[46] Absorption, Transport and Distribution of Vitamin E


- Metabolism of vitamin E during skin permeation
[6] Dermal penetration and systemic distribution of 14C-labeled vitamin E in human skin grafted athymic nude mice (only abstract available)

"In vivo percutaneous penetration and tissue distribution of 14C-labeled vitamin E applied to human skin grafted onto athymic nude mice were determined. At 1 hr, mouse skin contained the highest level of radioactivity, followed by the muscle, blood, liver, lung, adipose tissue, spleen, kidney, brain, heart, and eyes. A linear increase with time in tissue radioactivity was observed throughout the 24 hr experimental period. At 4 and 24 hrs skin grafts were highly radioactive. At 4 hrs the epidermis and the upper portion of the dermis contained more radioactivity than the remaining portion of the dermis. In contrast, at 24 hrs the highest level of radioactivity was detected in the lower dermis. No radioactivity was detected in expired air while 0.2% of the dose was found in the urine. The data show that vitamin E does penetrate skin and that the dermis acts as a barrier or reservoir for this highly lipophilic compound."​

- Penetration and distribution of α-tocopherol, α- or γ-tocotrienols applied individually onto murine skin


- Mechanisms for the prevention of vitamin E excess


- Inhibition of various glutathione S-transferase isoenzymes by RRR-α-tocopherol

- The Relationship Between Dose of Vitamin E and Suppression of Oxidative Stress in Humans


If someone has a light, do shine.



They didn't specify. I would make sure to not be insufficient on the other and it should be enough to prevent issues.

Lately, I am reacting poorly to any vitamin E supplement orally or topically.

 

[sunraiser]

Lately, I am reacting poorly to any vitamin E supplement orally or topically.

What kind of dosage are you taking?

@Amazoniac have you read this thread? https://raypeatforum.com/community/threads/vitamin-e-causes-all-sorts-of-negative-problems-according-to-this-article.21347/

I can't verify the validity as my understanding of vitamin E isn't very robust but I found the thread interesting. Maybe taking it orally presents some kind of challenge in the liver (like it's "used up" in rebalancing k2 or vitamin A levels in the liver?), where as transdermally this step is missed and it wreaks havoc on vitamin C levels?

Excess Vitamin E will also act as an oxidant instead of an anti-oxidant and in fact, doses of Vitamin E much above 140 milligrams will actually destroy the activity of Vitamin C.

Do you still notice a distinct benefit from oral vit E and at what kind of intake level?

 

[Amazoniac]

What kind of dosage are you taking?

@Amazoniac have you read this thread? https://raypeatforum.com/community/threads/vitamin-e-causes-all-sorts-of-negative-problems-according-to-this-article.21347/

I can't verify the validity as my understanding of vitamin E isn't very robust but I found the thread interesting. Maybe taking it orally presents some kind of challenge in the liver (like it's "used up" in rebalancing k2 or vitamin A levels in the liver?), where as transdermally this step is missed and it wreaks havoc on vitamin C levels?



Do you still notice a distinct benefit from oral vit E and at what kind of intake level?

Thanks for the consideration, I was destined to kitten videos.

The company is reluctant in informing the vitamin E content per bar, according to them it's a formula secret. But it's extracted from a natural source. The only irritation appears to be in my brain for not figuring this out.

A possible difference in tissue distribution is what led me to those 3 links above; when ingested it should be more regulated and the liver should partition it based on needs. Vitamin E having a much longer half of the lives than K and certain parts of the body having slower turnover, these added to skipping the regulatory step could perhaps set a good condition to deplete K locally making it difficult to replenish unless I leave it applied on the skin. It's something rare, so there has to be more to the story, but it points to a recycling issue.

Unfortunately vits C and K can only correct to a certain extent, otherwise I could just bathe in them and problem solved. It doesn't take too much exposure for the adverse effect from vitamin E to return.

I was also thinking about the possibility of Raj's antioxidative stress, maybe I could try NAC to rule this out.

--
From the first source of the previous post:

Spoiler

 

[sunraiser]

Thanks for the consideration, I was destined to kitten videos.

The company is reluctant in informing the vitamin E content per bar, according to them it's a formula secret. But it's extracted from a natural source. The only irritation appears to be in my brain for not figuring this out.

A possible difference in tissue distribution is what led me to those 3 links above; when ingested it should be more regulated and the liver should partition it based on needs. Vitamin E having a much longer half of the lives than K and certain parts of the body having slower turnover, these added to skipping the regulatory step could perhaps set a good condition to deplete K locally making it difficult to replenish unless I leave it applied on the skin. It's something rare, so there has to be more to the story, but it points to a recycling issue.

Unfortunately vits C and K can only correct to a certain extent, otherwise I could just bathe in them and problem solved. It doesn't take too much exposure for the adverse effect from vitamin E to return.

I was also thinking about the possibility of Raj's antioxidative stress, maybe I could try NAC to rule this out.

--
From the first source of the previous post:

Spoiler

View attachment 12009 View attachment 12010

That makes a lot of sense.

I tend to operate with far more of a skew towards the empirical so I don't have a study, but my experience with sunshine on skin has a similar correlation, although without negative (more just different kinds of positive) impact. A few months of sunshine in shorts and t-shirt brought 40-50ng/ml vit D levels, but after this proper sunbathing on torso and back brought about a huge change in wellbeing that was apparently separate from vitamin D status (the effects were only carried over a few days after the full sun exposure).

It might seem obvious but the area of application is clearly extremely important, and perhaps general liver health alongside cellular energy levels allow for higher or lower tolerance and rebound from transdermal application in a specific area, as you've implied.

I'm not sure we're designed to uptake fat solubles (aside from sunshine based vit D) transdermally in an effective manner - though robust people will be able to tolerate it to a far higher degree.

@haidut - this might seem a silly question as it's from wheat bran but could you confirm the approx amounts of a/b/d/g tocopherol in a serving? Would it be akin to googling the general ratios in wheat bran oil?

Also... I saw you refuted this elsewhere but I think it's interesting as an evidence source for people to consider. If they're consistently suppplementing something that favours alpha and not eating foods (like grains or nuts) that have a different balance of tocopherols then it's implausible to say an imbalance couldn't occur imo. Especially at supplemental levels (so possbily wise to stick to a very low dose or to not take every day).

"Despite promising evidence from in vitro experiments and observational studies, supplementation of diets with α-tocopherol has not reduced the risk of cardiovascular disease and cancer in most large-scale clinical trials. One plausible explanation is that the potential health benefits of α-tocopherol supplements are offset by deleterious changes in the bioavailability and/or bioactivity of other nutrients. We studied the effects of supplementing diets with RRR-α-tocopheryl acetate (400 IU/d) on serum concentrations of γ- and δ-tocopherol in a randomized, placebo-controlled trial in 184 adult nonsmokers. Outcomes were changes in serum concentrations of γ- and δ-tocopherol from baseline to the end of the 2-mo experimental period. Compared with placebo, supplementation with α-tocopherol reduced serum γ-tocopherol concentrations by a median change of 58% [95% CI = (51%, 66%), P < 0.0001], and reduced the number of individuals with detectable δ-tocopherol concentrations (P< 0.0001). Consistent with trial results were the results from baseline cross-sectional analyses, in which prior vitamin E supplement users had significantly lower serum γ-tocopherol than nonusers. In view of the potential benefits of γ- and δ-tocopherol, the efficacy of α-tocopherol supplementation may be reduced due to decreases in serum γ- and δ-tocopherol levels. Additional research is clearly warranted." (Huang & Appel, "Supplementation of Diets with α-Tocopherol Reduces Serum Concentrations of γ- and δ-Tocopherol in Humans", J. Nutr.October 1, 2003)

*

"In a cross-sectional survey of 86 elderly persons, it was observed that subjects with elevated plasma alpha-tocopherol levels had depressed plasma gamma-tocopherol. Tocopherols were measured by both reverse-phase and normal-phase high performance liquid chromatography (HPLC). When eight human volunteers (age range 30-60) were given 1200 IU of all-rac-alpha-tocopherol daily for 8 wk, plasma gamma-tocopherol and beta-tocopherol decreased in all subjects. After supplementation, gamma-tocopherol values were typically 30-50% of initial values, and alpha-tocopherol values were typically 200-400% of initial values. These results suggest that intestinal uptake and/or plasma transport make more efficient use of alpha-tocopherol than of gamma- or beta-tocopherol. Moreover, the results indicate that the ratio of gamma- to alpha-tocopherol in plasma would be a more satisfactory index to measure compliance in trials involving supplementation with alpha-tocopherol. (Handelman et al, "Oral alpha-tocopherol supplements decrease plasma gamma-tocopherol levels in humans", J Nutr, 1985)

 

[sunraiser]

I also wonder if full body sun exposure, assuming it's tolerated, drastically lowers the need for vitamin E as an anti-inflammatory and antioxidant in general? It could mean supplemental intakes in those circumstances do more harm than good!

 

[Amazoniac]

I also wonder if full body sun exposure, assuming it's tolerated, drastically lowers the need for vitamin E as an anti-inflammatory and antioxidant in general? It could mean supplemental intakes in those circumstances do more harm than good!

I amn't sure about that. It must help but at the same time the stress from radiation increases its requirements when it's needed to stabilize fats, and there can also be direct destruction when the sunny strikes the skin.

- Vitamin E and Skin Wealth

"Vitamin E is the most abundant lipophilic antioxidant found in human skin (1, 2). In humans, levels of vitamin E in the epidermis are higher than the dermis (1). Although the predominant form of vitamin E in skin of unsupplemented individuals is α-tocopherol, skin may also contain measurable amounts of γ-tocopherol (3) and other diet-derived tocopherols and tocotrienols (4)."

"Following oral ingestion, it takes at least seven days before the vitamin E content of sebum is altered (5, 7)."

"Exposures to UV light (3, 9, 10) or ozone (6, 11, 12) lower the vitamin E content in skin, primarily in the stratum corneum."

"[..]much of a topically applied dose of vitamin E alone will be destroyed in the skin following exposure to UV light (10). This suggests that although vitamin E is working as an antioxidant, it is unstable on its own and easily lost from the skin."

"Although molecules in the vitamin E family can absorb light in the UVB spectrum, the “sunscreen” activity of vitamin E is considered limited since it cannot absorb UVA light or light in higher wavelengths of the UVB spectrum (25). Thus, the primary photoprotective effect of vitamin E is attributed to its role as a lipid-soluble antioxidant."​

Regarding the puzzle, I have to ask myself:

Will is NAC for me?

☐ A nicht, nicht: no antioxidative stress
☐ An ach, ja: possible lack of recyclers
☐ Egal: something else​

- Nutritional Biochemistry of the Vitamins (978-0-511-07211-6)

"The retention of α-tocopherol in tissues varies. In the lungs the vitamin has a half-life of 7.6 days, in liver 9.8 days, in skin 23.4 days, in brain 29.4 days, and in the spinal cord 76.3 days (Ingold et al., 1987)."

"Most of the studies of the antioxidant activity of vitamin E have used relatively strong oxidants as the source of oxygen radicals to produce lipid peroxides in lipoproteins or liposomes in vitro. Studies of lipoproteins treated in vitro with low concentrations of sources of the perhydroxyl radical suggest that vitamin E may have a prooxidant action. Over 8 hours, there was 10-fold more formation of cholesterol ester hydroperoxide (an index of lipid peroxidation) in native LDL than in vitamin E-depleted LDL (Bowry et al., 1992). This is perhaps unsurprising; vitamin E and other radical-trapping antioxidants are effective because they form stable radicals that persist long enough to undergo reaction to nonradical products. It is therefore to be expected that they are also capable of perpetuating the radical chain reaction deeper into lipoproteins or membranes, as shown in Figure 4.5, therefore causing increased oxidative damage to lipids, especially in the absence of co-antioxidants such as ascorbate or ubiquinone (Upston et al., 1999; Carr et al., 2000)."

"The physiological role of vitamin E as an antioxidant and scavenger of free radicals explains the apparently complex nutritional interactions between vitamin E and selenium. Selenium is required, as the selenium analog of cysteine, selenocysteine, in the catalytic site of glutathione peroxidase. As noted previously, the membrane-specific isoenzyme of glutathione peroxidase catalyzes the reduction of the tocopheroxyl radical back to tocopherol. In addition, glutathione peroxidase reduces hydrogen peroxide and so lowers the amount of peroxide available for the generation of radicals, whereas vitamin E is involved in removing the products of attack by these radicals on lipids. Thus, in vitamin E deficiency, selenium has a beneficial effect in lowering the concentrations of alkylperoxyl radicals, and conversely, in selenium deficiency, vitamin E has a protective effect in reducing the radicals. When selenium is adequate, but vitamin E is deficient, tissues with low activity of glutathione peroxidase [e.g., the central nervous system and (rat) placenta] are especially susceptible to lipid peroxidation, whereas tissues with high activity of glutathione peroxidase are not. Conversely, with adequate vitamin E and inadequate selenium, membrane lipid peroxidation will be inhibited, but tissues with high peroxide production and low catalase activity will still be at risk from peroxidative damage, especially to sulfhydryl proteins."

"There may also be an effect of selenium deficiency on vitamin E nutrition. Selenium deficiency causes a specific pancreatic atrophy, which is unresponsive to vitamin E supplements. In turn, this leads to impaired secretion of lipase, and hence impaired absorption of dietary lipids in general that will affect the absorption of vitamin E (Thompson and Scott, 1970)."​

- The Fat-soluble vitamins (978-1-4615-8870-2)

Reinforcing our suspicion that it's somewhere between 0-100%.

"Vitamin E also has been reported to be interrelated with the nutrition and metabolism of vitamin A, iron, and a large number of other nutrients, notably

ascorbic acid (McCay et al., 1959),
vitamin D2 (Selye et al., 1964), -- Further studies on anacalciphylaxis
vitamin B12 (Oski et al., 1966),
thiamin (D'Agostino, 1952), -- Influence of alpha-tocopherol on urinary elimination of thiamine (?)
manganese (Lee et al., 1962), -- Rôle of manganese and vitamin E deficiency in mouse paralysis
and magnesium (Selisko, 1961). -- Magnesium - A vitamin E synergist?"
​

I'm posting this last part out of curiosity, because I don't think it's relevant to my case.

 

[milk_lover]

What kind of dosage are you taking?

@Amazoniac have you read this thread? https://raypeatforum.com/community/threads/vitamin-e-causes-all-sorts-of-negative-problems-according-to-this-article.21347/

I can't verify the validity as my understanding of vitamin E isn't very robust but I found the thread interesting. Maybe taking it orally presents some kind of challenge in the liver (like it's "used up" in rebalancing k2 or vitamin A levels in the liver?), where as transdermally this step is missed and it wreaks havoc on vitamin C levels?



Do you still notice a distinct benefit from oral vit E and at what kind of intake level?

I don't like the smell of tocovit, that's why I don't apply it on the skin anymore. Also, my cells kinda get filled with water when I apply it topically for some reason. I take it orally usually but I learned not to take a big dose as that messes up my digestion. I take 2 to 3 drops orally in days I suspect I ingested a lot of PUFA. Although I don't feel the best (vitamin D and K2 are much better suited for my body), I am hoping it's helping me fight against our worst enemy, PUFA.

 

[Amazoniac]

my cells kinda get filled with water when I apply it topically for some reason

Letters to the Editor | Original Internist

"The Shutes were cardiovascular specialists and arguably the major proponents of vitamin E use in the late 1940s. They recommended 1500 units of [] vitamin E, per day, for the rest of his life. Interestingly, the product was sold as a liquid versus the capsules we are familiar with.

I called Dr. Paul Eck, my resident nutritional expert, ready to next call the news media and tout the incredible scientific evidence of vitamin E's efficacy in circulation health. Much to my surprise, Dr. Eck rained on my parade with the words, 'Yes, Bill, but ... through hair mineral analysis, we know that vitamin E raises sodium in the body, through action on the adrenal cortex and aldosterone secretion. Sodium displaces calcium, eg, in water softeners. Sodium also renders calcium more soluble in times of stress and increased adrenal cortical activity.'"

I don't like the smell of tocovit

Is it the refined or the previous version?