Is Supplementing Vit E Actually Bad For You?

[Travis]

We now have 2 worthy Vit E supplements. High Gamma in MCT oil and dry Vit E succinate and both can be taken on the same day. So my original question "Is Supplementing Vitamin E actually bad for you" is NOT if you are taking the right kind. Choice your Vit E carefully...not synthetic and not in PUFA oil and not alpha only. This thread has been a great education on Vit E.

Yes: Taking 'vitamin E' is only harmful if you consume enough α-tocopherol to inhibit γ-tocopherol assimilation, yet taking them together is never a bad thing. The anticancer effect of vitamin E succinate however appears to be transcriptional, having little to do with α-tocopherol's classic functions and everything to do with calcium. Other calcium ionophores cause similar cell changes, and so does anything which increases intracellular cAMP. It has been shown that the 'calcium response element' is identical to the 'cAMP response element,' implying that cAMP activates transcription—through CREB—only to the degree that it increases intracellular calcium.

Sheng, M. "Membrane depolarization and calcium induce c-fos transcription via phosphorylation of transcription factor CREB." Neuron (1990)​

It has also been shown that the androgen receptor (AR) associates with CREB binding protein (CBP)—an unfortunate name since CREB already has 'binding protein' in its acronym, making the fully-expanded construct sound ridiculous (cAMP response element binding protein binding protein). The CBP increases the transcriptional activity of the androgen receptor by dimerizing with it, and it has been shown that other transcription factors compete for CBP (especially CREB).

Frønsdal, K. "CREB binding protein is a coactivator for the androgen receptor and mediates cross-talk with AP-1." Journal of Biological Chemistry (1998)​

So this is another way that Ca²⁺ should reduce the transcriptional activity of the androgen receptor, by inducing CREB's migration to the nucleus and subsequent CBP dimerization; since the amounts of this transcription factor are limited, this would mean that other transcription factors that normally heterodimerize with it—such as the androgen receptor—would have reduced activity for encoding certain genes. This could explain the reduced levels of androgen receptor mRNA after α-tocopherol succinate, and partially explain the reduced activity of the protein it encodes (which can partially be explained by Ca²⁺-dependent association of AR with calmodulin).

So intracellular Ca²⁺ reliably reduces androgen activity while it induces transcription of other genes, such as the Ca²⁺-related vitamin D receptor (VDR). Vitamin E succinate is a safe calcium ionophore, and even in the event of the succinate bond being cleaved-off it would still be available to inhibit lipid peroxidation in the membrane and mitochondria (with succinate being fed into the citric acid cycle). Since some α-tocopherol succinate would most certainly become α-tocopherol within the body, then taking γ-tocopherol at the same time would eliminate the only real negative side-effect of 'vitamin E.' Taking γ-tocopherol will also reliable reduce reactive nitrogen species:

Cooney, R. "Gamma-tocopherol detoxification of nitrogen dioxide: superiority to alpha-tocopherol." Proceedings of the National Academy of Sciences (1993)​

...subsequent prostaglandin formation:

Beharka, A. "Mechanism of vitamin E inhibition of cyclooxygenase activity in macrophages from old mice: role of peroxynitrite." Free Radical Biology and Medicine (2002)​

...and cancer consequent of prostaglandin formation:

Castellone, M. "Prostaglandin E₂ promotes colon cancer cell growth through a Gs-axin-ß-catenin signaling axis." Science (2005)
Campbell, S. "Development of gamma (γ)-tocopherol as a colorectal cancer chemopreventive agent." Critical reviews in oncology/hematology (2003)​

 

[Obi-wan]

Per @Travis B taking both High Gamma Vit E (MCT oil) and dry Vit E succinate is a 1, 2 Knock out punch. See also What Would You Suggest For BPH Prostate Trouble?

 

[Mauritio]

So can somebody please tell which Vitamin E i can still buy?
I have on that has mixed alpha-,beta- and gamma tocopherols and also tocotrienols but its diluted in sunflower oil ...

 

[Obi-wan]

So can somebody please tell which Vitamin E i can still buy?
I have on that has mixed alpha-,beta- and gamma tocopherols and also tocotrienols but its diluted in sunflower oil ...

High Gamma Vit E (MCT oil) with mixed alpha-,beta- and gamma tocopherols (Full Spectrum E) and also tocotrienols and dry Vit E succinate (Now)

 

[Mauritio]

High Gamma Vit E (MCT oil) with mixed alpha-,beta- and gamma tocopherols (Full Spectrum E) and also tocotrienols and dry Vit E succinate (Now)

thanks !

 

[Wagner83]

@Travis, did you come across anything which mentioned the particular anti-estrogenic effects of alpha-tocopherol which haidut hinted at? Wouldn't it be relevant for cancer and lung function?

[...]
The main anti-estrogenic effects are from alpha tocopherol, which has gotten some bad rep lately but it is the only isomer shown to act as estrogen receptor antagonist. The gamma, delta and beta tocopherols are mostly LOX inhibitors, which is a great benefit but not really directly related to estrogen. [...]

 

[haidut]

@Travis, did you come across anything which mentioned the particular anti-estrogenic effects of alpha-tocopherol which haidut hinted at? Wouldn't it be relevant for cancer and lung function?

Here are some relevant links.
https://raypeatforum.com/community/threads/vitamin-e-is-an-estrogen-receptor-antagonist.8506/
https://raypeatforum.com/community/...opherol-is-a-potent-aromatase-inhibitor.3106/

 

[Wagner83]

Here are some relevant links.
https://raypeatforum.com/community/threads/vitamin-e-is-an-estrogen-receptor-antagonist.8506/
https://raypeatforum.com/community/...opherol-is-a-potent-aromatase-inhibitor.3106/

Thanks, I saw an old thread of yours in which you had questioned if alpha-tocopherol really depleted gamma-tocopherol, since then I saw other posts which made me think that you now agree with Travis that indeed, alpha-tocopherol does deplete gamma-tocopherol when supplemented on its own (or with a high-ratio in its favor). What is your current opinion on the matter? I remember seeing you say you supplemented gamma one week, then alpha, and then mixed tocopherols (swanson older formula, not the present one).

 

[haidut]

Thanks, I saw an old thread of yours in which you had questioned if alpha-tocopherol really depleted gamma-tocopherol, since then I saw other posts which made me think that you now agree with Travis that indeed, alpha-tocopherol does deplete gamma-tocopherol when supplemented on its own (or with a high-ratio in its favor). What is your current opinion on the matter? I remember seeing you say you supplemented gamma one week, then alpha, and then mixed tocopherols (swanson older formula, not the present one).

I think if only alpha-toc is used in the long run it would probably lead to depletion of the other isomers. So, mixed tocopherols are probably best but I favor the high-alpha variety as the one found in wheat and sunflowers, as opposed to the high-gamma ones in soy, peanuts, etc. I think many of the positive studies with high-gamma are sponsored (or motivated) at least partially by the soy industry which has a lot of waste product to sell. Similar to the fish oil scam but this time the tocopherols are actually good for us. The vast majority of the older studies with vitamin E used a high-alpha variety, and some of them used pure alpha-tocopherol. The gamma tocopherol science is very recent and not very industry-independent. So, I don't trust is enough yet

 

[lollipop]

I think if only alpha-toc is used in the long run it would probably lead to depletion of the other isomers. So, mixed tocopherols are probably best but I favor the high-alpha variety as the one found in wheat and sunflowers, as opposed to the high-gamma ones in soy, peanuts, etc. I think many of the positive studies with high-gamma are sponsored (or motivated) at least partially by the soy industry which has a lot of waste product to sell. Similar to the fish oil scam but this time the tocopherols are actually good for us. The vast majority of the older studies with vitamin E used a high-alpha variety, and some of them used pure alpha-tocopherol. The gamma tocopherol science is very recent and not very industry-independent. So, I don't trust is enough yet

Very interesting.

 

[Obi-wan]

But @Travis has given us a lot of evidence on this forum regarding gamma superiority...also alpha succinate and just recently tocotrienols. And I think we can all agree that the carrier should not be a PUFA oil...

 

[Wagner83]

I think if only alpha-toc is used in the long run it would probably lead to depletion of the other isomers. So, mixed tocopherols are probably best but I favor the high-alpha variety as the one found in wheat and sunflowers, as opposed to the high-gamma ones in soy, peanuts, etc. I think many of the positive studies with high-gamma are sponsored (or motivated) at least partially by the soy industry which has a lot of waste product to sell. Similar to the fish oil scam but this time the tocopherols are actually good for us. The vast majority of the older studies with vitamin E used a high-alpha variety, and some of them used pure alpha-tocopherol. The gamma tocopherol science is very recent and not very industry-independent. So, I don't trust is enough yet

Ok, what about the wheat industry, wouldn't they fund pro alpha-tocopherols studies? Is there any information in particular that you saw and which made you convinced the soy industry is funding studies and making propaganda against the wheat derived vitamin e?
The mixed tocopherols high in alpha-tocopherols could still provide 3 times * the amount of gamma, given that supplemental alpha-tocopherols on their own deplete other isomers, where do you think the line is between depletion or no depletion?

* Tocovit isomers, as per yourself https://raypeatforum.com/community/...actually-bad-for-you.22626/page-5#post-320102

 

[haidut]

But @Travis has given us a lot of evidence on this forum regarding gamma superiority...also alpha succinate and just recently tocotrienols. And I think we can all agree that the carrier should not be a PUFA oil...

I did not say I would not use it. I said I prefer mixed tocopherols with high alpha content so that the emphasis is on estrogen antagonism, but gamma tocopherol still has a very important role due to LOX/COX inhbition.

 

[haidut]

Ok, what about the wheat industry, wouldn't they fund pro alpha-tocopherols studies? Is there any information in particular that you saw and which made you convinced the soy industry is funding studies and making propaganda against the wheat derived vitamin e?
The mixed tocopherols high in alpha-tocopherols could still provide 3 times * the amount of gamma, given that supplemental alpha-tocopherols on their own deplete other isomers, where do you think the line is between depletion or no depletion?

* Tocovit isomers, as per yourself https://raypeatforum.com/community/...actually-bad-for-you.22626/page-5#post-320102

The wheat industry is not nearly as powerful as the soy/corn industry. There is a reason vitamin E from wheat germ oil disappeared and was replaced by high-gamma version - i.e. the high-alpha variety is much more expensive to make. If you check several bulk vendors who provide all of the vitamins, you will see that alpha tocopherol is usually 2-3 times more expensive than the gamma isomer. There is a reason for that, and it's not just production costs.
Anyways, I did not say I would not use gamma isomer. I said that I prefer high-alpha varieties so that the emphasis is on estrogen antagonism. The gamma isomer is still needed for its LOX/COX inhbition.

 

[Wagner83]

The wheat industry is not nearly as powerful as the soy/corn industry. There is a reason vitamin E from wheat germ oil disappeared and was replaced by high-gamma version - i.e. the high-alpha variety is much more expensive to make. If you check several bulk vendors who provide all of the vitamins, you will see that alpha tocopherol is usually 2-3 times more expensive than the gamma isomer. There is a reason for that, and it's not just production costs.
Anyways, I did not say I would not use gamma isomer. I said that I prefer high-alpha varieties so that the emphasis is on estrogen antagonism. The gamma isomer is still needed for its LOX/COX inhbition.

OK thanks.

I had understood, but this also means that you wouldn't want to deplete gamma in the body either, so the question of which percentage of alpha-tocopherols does deplete the other ones is important. Perhaps simply adding a high gamma one on other days would be good enough.

 

[haidut]

OK thanks.

I had understood, but this also means that you wouldn't want to deplete gamma in the body either, so the question of which percentage of alpha-tocopherols do deplete the other ones is important. Perhaps simply adding a high gamma one on other days would be good enough.

A mixed tocopherol with high-alpha content will not deplete gamma. It will just have more alpha-centric effects. Only taking pure alpha tocopherol with nothing else has so far been shown to deplete the other isomers.

 

[Travis]

@Travis, did you come across anything which mentioned the particular anti-estrogenic effects of alpha-tocopherol which haidut hinted at? Wouldn't it be relevant for cancer and lung function?

I did come across one interesting study on this effect but now I cannot find it. It seems apparent that tocopherols are unique in their influence on the estrogen receptor, with α-tocopherol exhibiting the greatest potency in this regard. This is implied by α-tocopherol's increased potency in the the rat fetal absorption assay, a property which had given the α-congener primacy starting in the 1940s. Results from these early studies and αlpha's more efficient transport in the body had led to the view that β-, γ-, and δ-tocopherols were merely 'less-active vitamin E types.' However, γ-tocopherol can adduct-with reactive nitrogen species—a powerful non-vitamin function.

This interaction with the estrogen receptor is of course more directly demonstrated by the study that you'd linked, although this experiment does not compare α-tocopherol with any other type.

Chamras, Hilda. "Novel interactions of vitamin E and estrogen in breast cancer." Nutrition and cancer (2005)​

'Interestingly, when estrogen was absent in the medium, vitamin E induced a slight growth stimulation rather than inhibition in both MCF-7 and T47D cell lines.' —Chamras​

They had used all-racemic α-tocopherol, an approximately equal blend of 8 distinct α-tocopherol stereoisomers (seven of which are unnatural). All-racemic α-tocopherol appears capable at antagonizing both estradiol and tamoxifen, an E₂ analogue, at high concentrations. Gamma- and δ-tocopherol have also been shown to inhibit mammary carcinogenesis in the rat, although this had been a nitrosamine-induced cancer:

Smolarek, Amanda. "Dietary tocopherols inhibit cell proliferation, regulate expression of ERα, PPARγ, and Nrf2, and decrease serum inflammatory markers during the development of mammary hyperplasia." Molecular carcinogenesis (2013)

Smolarek, Amanda. "Dietary administration of δ-and γ-tocopherol inhibits tumorigenesis in the animal model of estrogen receptor–positive, but not HER-2 breast cancer." Cancer Prevention Research (2012)​

Nitrosamines could perhaps work by releasing the nitrosonium ion, which could travel to the nucleus and nitrosylate dNA. Of course, any cancer induced by reactive nitrogen species would be better inhibited by γ- and δ-tocopherols—as they've been shown to do.

'Nitrotyrosine is a known marker for nitrosative stress. In the mammary gland, the dietary administration of δ-tocopherol, γ-tocopherol and γ-TmT resulted in a decrease of nitrotyrosine levels by 14%, 18%, and 19%, respectively. The level of 8-oxo-dG, a marker of oxidative stress, was also decreased by treatment with δ-tocopherol (10%), γ-tocopherol (21%) and γ-TmT (14%); however the results were not statistically significant. Levels of 8-oxo-dG and nitrotyrosine were not reduced by α-tocopherol in the mammary gland.' —Smolarek

'When compared to the E₂ control group, treatment with 0.5% γ-TmT for 2 wk significantly decreased E₂ serum levels to 45.3 pg/ml.' —Smolarek​

​

'Serum levels of PGE₂ were decreased by γ-TmT treatment, with which significant reduction of serum PGE₂ was shown by 10-wk treatment with 0.5% γ-TmT by 71%.' —Smolarek

'As compared to the control group, dietary administration of δ- and γ-tocopherol reduced tumor burden by 32% and 33%, respectively, but α-tocopherol-enriched diet had no effect. Tumor multiplicity for the control group was 5.0 ± 0.1 and was decreased by treatment with δ-tocopherol (2.9 ± 0.1), γ-tocopherol (3.4 ± 0.1), and γ-TmT (3.9 ± 0.1) which translates to 42%, 32%, and 22% inhibition, respectively.' —Smolarek​

Delta- and γ-tocopherol have a free space on the chromanol ring, allowing them to adduct-with reactive nitrogen species; this has been demonstrated in the case of nitrogen dioxide and peroxynitrite, although it could perhaps bind others. Inhibiting reactive nitrogen species is inhibiting protein nitrosylation, dNA nitrosylation, and also prostaglandins since peroxynitrite is a substrate for cyclooxygenase-2.

Yet α-tocopherol does appear to have increased potency at promoting rat fertility, although β-tocopherol has approximately half the activity.

Søndergaard, Helge. "Biological activity of vitamin E compounds and natural materials by the resorption-gestation test, and chemical determination of the vitamin E activity in foods and feeds." The Journal of nutrition (1977)​

'The biological activity of the tocopherols and tocotrienols has been re-examined by the rat resorption-gestation test. The following values have been obtained (with d,l-α-tocopheryl acetate = 100%): d-α-tocopherol 80%; d,l-α-tocopherol 59%; d-α-tocopheryl acetate 136%; d-α-tocotrienol 13%; d-β-tocopherol 45%; d-β-tocotrienol 4%; d-γ-tocopherol 13%; d-δ-tocopherol less than 0.4%. The possibility of α- and γ-tocopherol being synergists has been tested, but no significant effect was found.' ―Søndergaard​

So besides the physical–chemical function that γ-tocopherol displays, α-tocopheryl appears to have almost hormonal effects. Whether this has something to do with its effect on the estrogen receptor or its enhanced bioavailability could be debatable; alpha-tocopherol is also slightly more effective than the others at stopping free radical chain reactions.

However, both α-tocotrienol and α-tocopheryl succinate appear to work completely independently of the estrogen receptor—perhaps implying that the steric structure of α-tocopherol has more relevance than the electronic properties of its chromanol 'head' group, which is shared among all α-forms. The differential properties of vitamin E isomers, congeners, and carboxylic acid esters appear consistent with a receptor–ligand interaction specific to d-α-tocopherol.

Nesaretnam, Kalanithi. "Tocotrienols inhibit the growth of human breast cancer cells irrespective of estrogen receptor status." Lipids (1998)

Chamras, Hilda. "Novel interactions of vitamin E and estrogen in breast cancer." Nutrition and cancer (2005)

'Many in vitro studies support the hypothesis that vitamin E (α-tocopherol) and vitamin E succinate (VES) inhibit cell growth in breast cancer cell lines. The mechanism(s) of this suppression of cancer cell proliferation is not understood. Due to the high hydrophobicity of vitamin E, VES has been used as a source of vitamin E in the most recent studies. However, the inhibitory effect of VES on breast cancer cell growth was mostly studied using ER-negative MDA-MB-231 cells. Schwartz and Shklar studied human cancer cell lines, including an ER-positive breast cancer cell line, and found a 95% decrease in proliferation of α-tocopherol–treated MCF-7 cells compared with normal cells. Charpentier et al. demonstrated that VES inhibited ER-positive and -negative breast cancer cell lines in a dose-dependent manner in vitro. However, these authors reported that VES was the only form of vitamin E that inhibited cell proliferation, and the antiproliferative properties of VES were not due to the antioxidant effect. Notably, in their study, cells were incubated for a shorter period of time and with a lower concentration of vitamin E (15 µg/ml). In agreement with these authors, we found that VES is more inhibitory in ER-negative cells than in ER-positive cells. Malafa and Neitzel reported recently that VES inhibited the growth of MDA-MB-231 cells in nude mice. Also, VES was found to inhibit vascular endothelial growth factor gene expression in MDA-MB-231 cells. However, in their in vitro study, Malafa and Neitzel reported that VES decreased both MCF-7 and MDA-MB-231 cell viability along with an increase of cell apoptosis in MDA-MB-231 cells but no effect on apoptosis of MCF-7 cells. These results suggest that VES may inhibit cell growth by different pathways in different cell lines. In that respect, we found that ER-positive cells are more sensitive to vitamin E than to VES. On the contrary, ER-negative cells are inhibited more by VES than by vitamin E, suggesting the possibility of two different pathways of cell growth inhibition by vitamin E and VES.' ―Chamras​

 

[Wagner83]

I did come across one interesting study on this effect but now I cannot find it. It seems apparent that tocopherols are unique in their influence on the estrogen receptor, with α-tocopherol exhibiting the greatest potency in this regard. This is implied by α-tocopherol's increased potency in the the rat fetal absorption assay, a property which had given the α-congener primacy starting in the 1940s. Results from these early studies and αlpha's more efficient transport in the body had led to the view that β-, γ-, and δ-tocopherols were merely 'less-active vitamin E types.' However, γ-tocopherol can adduct-with reactive nitrogen species—a powerful non-vitamin function.

This interaction with the estrogen receptor is of course more directly demonstrated by the study that you'd linked, although this experiment does not compare α-tocopherol with any other type.

Chamras, Hilda. "Novel interactions of vitamin E and estrogen in breast cancer." Nutrition and cancer (2005)​

'Interestingly, when estrogen was absent in the medium, vitamin E induced a slight growth stimulation rather than inhibition in both MCF-7 and T47D cell lines.' —Chamras​

They had used all-racemic α-tocopherol, an approximately equal blend of 8 distinct α-tocopherol stereoisomers (seven of which are unnatural). All-racemic α-tocopherol appears capable at antagonizing both estradiol and tamoxifen, an E₂ analogue, at high concentrations. Gamma- and δ-tocopherol have also been shown to inhibit mammary carcinogenesis in the rat, although this had been a nitrosamine-induced cancer:

Smolarek, Amanda. "Dietary tocopherols inhibit cell proliferation, regulate expression of ERα, PPARγ, and Nrf2, and decrease serum inflammatory markers during the development of mammary hyperplasia." Molecular carcinogenesis (2013)

Smolarek, Amanda. "Dietary administration of δ-and γ-tocopherol inhibits tumorigenesis in the animal model of estrogen receptor–positive, but not HER-2 breast cancer." Cancer Prevention Research (2012)​

Nitrosamines could perhaps work by releasing the nitrosonium ion, which could travel to the nucleus and nitrosylate dNA. Of course, any cancer induced by reactive nitrogen species would be better inhibited by γ- and δ-tocopherols—as they've been shown to do.

'Nitrotyrosine is a known marker for nitrosative stress. In the mammary gland, the dietary administration of δ-tocopherol, γ-tocopherol and γ-TmT resulted in a decrease of nitrotyrosine levels by 14%, 18%, and 19%, respectively. The level of 8-oxo-dG, a marker of oxidative stress, was also decreased by treatment with δ-tocopherol (10%), γ-tocopherol (21%) and γ-TmT (14%); however the results were not statistically significant. Levels of 8-oxo-dG and nitrotyrosine were not reduced by α-tocopherol in the mammary gland.' —Smolarek

'When compared to the E₂ control group, treatment with 0.5% γ-TmT for 2 wk significantly decreased E₂ serum levels to 45.3 pg/ml.' —Smolarek​

View attachment 9923​

'Serum levels of PGE₂ were decreased by γ-TmT treatment, with which significant reduction of serum PGE₂ was shown by 10-wk treatment with 0.5% γ-TmT by 71%.' —Smolarek

'As compared to the control group, dietary administration of δ- and γ-tocopherol reduced tumor burden by 32% and 33%, respectively, but α-tocopherol-enriched diet had no effect. Tumor multiplicity for the control group was 5.0 ± 0.1 and was decreased by treatment with δ-tocopherol (2.9 ± 0.1), γ-tocopherol (3.4 ± 0.1), and γ-TmT (3.9 ± 0.1) which translates to 42%, 32%, and 22% inhibition, respectively.' —Smolarek​

Delta- and γ-tocopherol have a free space on the chromanol ring, allowing them to adduct-with reactive nitrogen species; this has been demonstrated in the case of nitrogen dioxide and peroxynitrite, although it could perhaps bind others. Inhibiting reactive nitrogen species is inhibiting protein nitrosylation, dNA nitrosylation, and also prostaglandins since peroxynitrite is a substrate for cyclooxygenase-2.

Yet α-tocopherol does appear to have increased potency at promoting rat fertility, although β-tocopherol has approximately half the activity.

Søndergaard, Helge. "Biological activity of vitamin E compounds and natural materials by the resorption-gestation test, and chemical determination of the vitamin E activity in foods and feeds." The Journal of nutrition (1977)​

'The biological activity of the tocopherols and tocotrienols has been re-examined by the rat resorption-gestation test. The following values have been obtained (with d,l-α-tocopheryl acetate = 100%): d-α-tocopherol 80%; d,l-α-tocopherol 59%; d-α-tocopheryl acetate 136%; d-α-tocotrienol 13%; d-β-tocopherol 45%; d-β-tocotrienol 4%; d-γ-tocopherol 13%; d-δ-tocopherol less than 0.4%. The possibility of α- and γ-tocopherol being synergists has been tested, but no significant effect was found.' ―Søndergaard​

So besides the physical–chemical function that γ-tocopherol displays, α-tocopheryl appears to have almost hormonal effects. Whether this has something to do with its effect on the estrogen receptor or its enhanced bioavailability could be debatable; alpha-tocopherol is also slightly more effective than the others at stopping free radical chain reactions.

However, both α-tocotrienol and α-tocopheryl succinate appear to work completely independently of the estrogen receptor—perhaps implying that the steric structure of α-tocopherol has more relevance than the electronic properties of its chromanol 'head' group, which is shared among all α-forms. The differential properties of vitamin E isomers, congeners, and carboxylic acid esters appear consistent with a receptor–ligand interaction specific to d-α-tocopherol.

Nesaretnam, Kalanithi. "Tocotrienols inhibit the growth of human breast cancer cells irrespective of estrogen receptor status." Lipids (1998)

Chamras, Hilda. "Novel interactions of vitamin E and estrogen in breast cancer." Nutrition and cancer (2005)

'Many in vitro studies support the hypothesis that vitamin E (α-tocopherol) and vitamin E succinate (VES) inhibit cell growth in breast cancer cell lines. The mechanism(s) of this suppression of cancer cell proliferation is not understood. Due to the high hydrophobicity of vitamin E, VES has been used as a source of vitamin E in the most recent studies. However, the inhibitory effect of VES on breast cancer cell growth was mostly studied using ER-negative MDA-MB-231 cells. Schwartz and Shklar studied human cancer cell lines, including an ER-positive breast cancer cell line, and found a 95% decrease in proliferation of α-tocopherol–treated MCF-7 cells compared with normal cells. Charpentier et al. demonstrated that VES inhibited ER-positive and -negative breast cancer cell lines in a dose-dependent manner in vitro. However, these authors reported that VES was the only form of vitamin E that inhibited cell proliferation, and the antiproliferative properties of VES were not due to the antioxidant effect. Notably, in their study, cells were incubated for a shorter period of time and with a lower concentration of vitamin E (15 µg/ml). In agreement with these authors, we found that VES is more inhibitory in ER-negative cells than in ER-positive cells. Malafa and Neitzel reported recently that VES inhibited the growth of MDA-MB-231 cells in nude mice. Also, VES was found to inhibit vascular endothelial growth factor gene expression in MDA-MB-231 cells. However, in their in vitro study, Malafa and Neitzel reported that VES decreased both MCF-7 and MDA-MB-231 cell viability along with an increase of cell apoptosis in MDA-MB-231 cells but no effect on apoptosis of MCF-7 cells. These results suggest that VES may inhibit cell growth by different pathways in different cell lines. In that respect, we found that ER-positive cells are more sensitive to vitamin E than to VES. On the contrary, ER-negative cells are inhibited more by VES than by vitamin E, suggesting the possibility of two different pathways of cell growth inhibition by vitamin E and VES.' ―Chamras​

Thanks for the thorough reply, it sounds like whatever the tocopherol, it has good effects. As for the alpha-tocopherol succinate, could it simply have to do with succinic acid? X-Ray has spoken in its favor.

Do you have any idea what alpha-/gamma-tocopherol ratio would prevent the gamma-tocopherol from being depleted? I recall reading in this thread that you would yourself pick a high gamma supplement, particularly regarding lung disease prevention from smoking, but like haidut said, I haven't seen anything which suggests a high ratio of alpha to gamma tocopherols is an issue in the long-term.

 

[Travis]

Thanks for the thorough reply, it sounds like whatever the tocopherol, it has good effects. As for the alpha-tocopherol succinate, could it simply have to do with succinic acid? X-Ray has spoken in its favor.

Do you have any idea what alpha-/gamma-tocopherol ratio would prevent the gamma-tocopherol from being depleted? I recall reading in this thread that you would yourself pick a high gamma supplement, particularly regarding lung disease prevention from smoking, but like haidut said, I haven't seen anything which suggests a high ratio of alpha to gamma tocopherols is an issue in the long-term.

I think part of the reason why tissue concentrations of α are always found greater than those of γ, despite approximately equal intakes between the two, is because of the latter's increased turnover. I think the turnover rate of γ-tocopherol could occur as a function of nitric oxide concentration, so people taking L-arginine or smoking might want a high-gamma blend.

I would like some γ-tocotrienol, but it's like $20 per milligram.

I think α-tocopheryl succinate works as a calcium ionophore. Just take a look at a few studies that show how it interacts with calcium and I think you'll agree. Succinate is a dicarboxylic acid, and all dicarboxylic acids chelate calcium as long as the carboxylate groups are close enough. Vitamin K regulates calcium in this manner: This cofactor helps to create dicarboxylic γ-carboxylglutamate modifications on proteins, chaperoning calcium and keeping it from precipitating in the plasma.

 

[Obi-wan]

$42.99