Is Supplementing Vit E Actually Bad For You?

schultz

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Not sure if something like this has been posted yet. I saw it in a paper and thought it was a nice little chart. Presumably extracted vitamin e from these oils would keep the same profile.

VitaminE.jpg
 

Travis

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Not sure if something like this has been posted yet. I saw it in a paper and thought it was a nice little chart. Presumably extracted vitamin e from these oils would keep the same profile.

View attachment 8740
That is a nice chart. I like the look of palm oil if you also consider the content of γ-tocotrienol, which has a prenylated tail but the same ṄO-scavenging head group. I haven't read about the cellular distribution of the tocotrienols yet, but I think you can assume on the character of their tail that they'd partition more intracellularly—perhaps being more associated with the mitochondria and less with the cell membrane (I should look into this). Perhaps it would also be good to post the fatty acid speciation of palm oil for quick reference:

palm3.png


palm2.png


palm.jpg


Looks like the ranges are somewhat somewhat consistent, with the first and third tables conforming to the ranges reported in the second. The most prevalent seems to be more-or-less a coin-toss between either oleic acid or, predictably, palmitic acid. Perhaps this plant has a desaturase enzyme?—converting stearate into oleate according to temperature? This does happen in our livers all the time, so even if we avoid oleic entirely we still get some. There even exists an intracellular enzyme, stearoyl–CoA desaturase, which makes this conversion using newly synthesized stearic acid conjugated with coenzyme A. The transcription of this enzyme is under genetic control, and it is most powerfully upregulated by estradiol (a 7× induction has been found in one study). Also, oleic acid will not spontaneously oxidize as it lacks the bis-allyl hydrogen characteristic of many polyunsaturated fatty acids. The hydrogen between two double bonds is far more easily-abstracted, and hence more prone to the initiatation step of peroxidation, than one adjacent to only one double bond. However, oleic acid could have unique serotonergic effects. Oleic acid amide, or oleamide, is a powerful and specific allosteric regulator of three serotonin receptors—5-HT₁, 5-HT₂, and 5-HT₇—and will powerfully induce sleep in low very concentrations. It does not effect serotonin binding, but binds to an adjacent site where it has been found to potentiate serotonin's response (on 5-HT₂) by over 500% (in nanomolar concentrations). This is not an 'agonist' nor is it an 'antagonist;' the words 'potentiator' and 'attenuator' would be more appropriate to describe oleamide. The most surprising thing is that the selectivity: Essentially only the amide of oleic acid can do this in low concentrations, all others having far less potency; even studies which had used over 30 modifications of the oleamide structure have failed to find one stronger. It has been shown that circulating oleic acid will enter the brain, and I think oleamide could partialy explain 'Italian psychology:' dramatic behavior, over-emotionality, impulsiveness, rudeness, and absurd language are all Italian archetypes (see Goodfellas);⁽¹⁾⁽²⁾⁽³⁾ the list of famous scientists who claim Italy as a homeland is disproportionately small. But what the high-sertotonin brain lacks in logic it can make-up for in poetry, music, and art. (I'm a German descendant myself, and like the Peter Duesberg's personality much more than his unscrupulous Italian rival: Robert Gallo.)

But the linoleic acid content should probably limit palm oil consumption to low levels anyhow, regardless of its favorable γ-tocopherol and -trienol concentrations—although this oil is obviously still far better than the majority of seed oils.

[1] Vincent, Frank. "Now go home and get your ******* shinebox." Goodfellas (1990)
[2] Bracco, Lorraine. "Wake up Henry." Goodfellas (1990)
[3] Pesci, Joe. "I'm funny how?" Goodfellas (1990)

 
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allblues

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@Travis Interesting thoughts on the serotonin-emotion-creativity interface. Anecdotally, being put on SSRI's as an anxious 17-year old really exploded my interest in art, especially classical music, something that's gradually faded after coming off them and especially since using serotonin antagonists. I sort of miss it; what I don't miss however, are the prolactin breast itches.

Great stuff on olive oil and the italians; if your posts start containing words like "youse," and recommendations of tomato sauce over pineapples, we'll know the tryptophan experiment has started!
 

Travis

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@Travis Interesting thoughts on the serotonin-emotion-creativity interface. Anecdotally, being put on SSRI's as an anxious 17-year old really exploded my interest in art, especially classical music, something that's gradually faded after coming off them and especially since using serotonin antagonists. I sort of miss it; what I don't miss however, are the prolactin breast itches.
Perhaps you should listen to Terrence McKenna if you haven't already. He has experimented with indoles like dimethyltrypamine and LSD (the ergoline ring actually has an indole buried within it). These are drugs which indisputably activate serotonin receptors, and I think Terrence McKenna mostly operates under the serotonin circuitry (and has quite a bit of experience in perturbing it). He's very linguistic but he's not a very rigorous logician, most of the time, and I think he very often fails when it comes to logic and hard science—which I think are perhaps more low-serotonin head states, and could have a bit more to do with histamine and dopamine.

I think this could make sense in a feeding-time sort-of-way, as our brains do appear sense food intake through tryptophan. Serotonin releases growth hormone, causes postprandial fatigue, post-exercise fatigue (as tryptophan is released from muscle), and appears to generally make for a more contented state. But this is often seen as 'laziness' by some, and perhaps wouldn't be practical state to be commonly found in. I think early stages of alcohol consumption are related to elevated serotonin—before the general anesthetic effects kick-in—and there is quite a bit of evidence for this. (But not to be confused with chronic alcoholic intake which is often characterized by low serotonin due to impaired tryptophan metabolism, a consequent of liver damage).

Yoshimoto, K. "Alcohol stimulates the release of dopamine and serotonin in the nucleus accumbens." Alcohol (1992)

'Only the 100 mM concentration of ethanol altered the extracellular levels of 5-HT (2-fold increase), dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid.' ―Yoshimoto

try.png click to embiggen
Great stuff on olive oil and the italians; if your posts start containing words like "youse," and recommendations of tomato sauce over pineapples, we'll know the tryptophan experiment has started!
Lol. I hope I never consume enough tryptophan and oleic acid at one time to start enjoying The Four Seasons. FFS! Everytime I hear that scoochi' song 'Sherry' it makes me want to strangle a puppy. (If I had my way that Frankie Valli would be sleepin' with the fishes.)
 
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Travis

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I have started to test this one but I asked the manufacturer to verify what it is...
Nice. I smoke about 12 cigarettes per day so I should really need to start using that stuff—perhaps even check the ratios found in the foods I eat. I noticed on the chart above that otherwise perfect coconut oil has literally '0% γ-tocopherol' (although is does have some δ-toco to offset the α-toco). As the lungs experience the most nitrogen radical exposure, it follows that this should be the most important place to have the proper γ∶α ratio. There are some good lung cancer rat studies ou there using γ-tocopherol specifically, and I think I might check those out pretty soon here (not that I'm overly concerned about it or anything, smoking 100% natural).. .
 
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Obi-wan

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Per Ray- A possible mitochondrial site for toxicity: In 1971 I was trying to combine some of the ideas of Albert Szent-Gyorgyi, Otto Warburg, W. F. Koch, and L. C. Strong. I was interested in the role of ubiquinone in mitochondrial respiration. In one experiment, I was using paper chromatography to compare oils that I had extracted from liver with vitamin E and with commercially purified ubiquinone. Besides using the pure substances, I decided to combine vitamin E with ubiquinone for another test spot. As soon as I combined the two oils, their amber and orange colors turned to an inky, greenish black color. I tested both bacterial and mammalian ubiquinone, and benzoquinone, and they all produced similar colors with vitamin E. When I ran the solvent up the paper, the vitamin E and the ubiquinone traveled at slightly different speeds. The black spot, containing the mixture, also moved, but each substance moved at its own speed, and as the materials separated, their original lighter colors reappeared. Charge-transfer bonds, which characteristically produce dark colors, are very weak bonds. I think this must have been that kind of bond. Years later, I tried to repeat the experiment, using "ubiquinone" from various capsules that were sold for medical use. Instead of the waxy yellow-orange material I had used before, these capsules contained a liquid oil with a somewhat yellow color. Very likely, the ubiquinone was dissolved in vegetable oil. At the time, I was puzzled that the color reaction didn't occur, but later I realized that a solvent containing double bonds (e.g., soy oil or other oil containing PUFA) would very likely prevent the close association between vitamin E and ubiquinone which is necessary for charge-transfer to occur. Since I think Koch and Szent-Gyorgyi were right in believing that electronic activation is the most important feature of the living state, I think the very specific electronic interaction between vitamin E and ubiquinone must play an important role in the respiratory function of ubiquinone. Ubiquinone is known to be a part of the electron transport chain which can leak electrons, so this might be one of the ways in which vitamin E can prevent the formation of toxic free-radicals. If it can prevent the "leakage" of electrons, then this in itself would improve respiratory efficiency. If unsaturated oils interfere with this very specific but delicate bond, then this could explain, at least partly, their toxicity for mitochondria. ["Electron leak" reference: B. Halliwell, in Age Pigments (R. S. Sohal, ed.), pp. 1-62, Elsevier, Amsterdam, 1981.]


Still having a hard time believing any Vit. E in a yellow color capsule is beneficial.
 
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Obi-wan

Obi-wan

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Per Ray- Olive oil is not a strong tumor promoter, but in some experiments it does have a slightly permissive effect on tumor growth.
 
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Obi-wan

Obi-wan

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More from Peat-

Besides antagonizing some of the end effects of the toxic fatty acids, vitamin E inhibits lipolysis, lowering the concentration of free fatty acids (the opposite of estrogen’s effect), and it also binds to, and inactivates, free fatty acids. The long saturated carbon chain is very important for its full functioning, and this saturated chain might allow it to serve as a substitute for the omega -9 fats, from which the Mead acid is formed. The unsaturated tocotrienols have hardly been tested for the spectrum of true vitamin E activity, and animal studies have suggested that it may be toxic, since it caused liver enlargement.

One possibly crucial protective effect of vitamin E against the polyunsaturated fatty acids that hasn't been explored is the direct destruction of linolenic and linoleic acid. It is known that bacterial vitamin E is involved in the saturation of unsaturated fatty acids, and it is also known that intestinal bacteria turn linoleic and linolenic acids into the fully saturated stearic acid.

"No metabolic function is known for alpha-tocopherolquinol or its quinone other than as a cofactor in the biohydrogenation of unsaturated fatty acids that can be carried out by only a few organisms."

P.E. Hughes and S.B. Tove, 1982.

“Linoleic acid was significantly decreased (P < 0.001) and there was a significant rise (P < 0.05) in its hydrogenation product, stearic acid. Linolenic acid was also significantly decreased. . . .” “The study provides evidence that bacteria from the human colon can hydrogenate C18 essential polyunsaturated fatty acids.”

F.A. Howard & C. Henderson, 1999

Because of the way in which the decision to call vitamin E a simple antioxidant was conditioned by the historical setting, there has been a reluctance, until recently, to give much weight to the pathogenicity of lipid peroxidation and free radicals, partly because lipid peroxidation is only a minor part of the toxicity of the polyunsaturated oils, and there was little support for the investigation of the real nature of their toxicity. This environment has even distorted the actual antioxidant value of the various forms of vitamin E. (For example, see Chen, et al., 2002.)

The people who say that vitamin E is nothing but an antioxidant sometimes take other antioxidants, with, or instead of, vitamin E. BHT, BHA, and many natural compounds (derived from industrial and agricultural wastes) are often said to be "better than vitamin E" as antioxidants. Anything that can be oxidized and reduced (melatonin, estrogen, tryptophan, carotene, etc.) will function as an antioxidant in some system, but in other circumstances, it can be a pro-oxidant.

The people who think there is benefit in the abstract "antioxidant" function seem to be thinking in terms of something that will, like a ubiquitous fire department, put out every little fire as soon as it starts. I think it's more appropriate to think of the biological antioxidant systems as programs for controlling the arsonists before they can set the fires.

Since the requirement for vitamin E decreases as the consumption of unsaturated fats decreases, the requirement, if any, would be very small if we didn't eat significant quantities of those fats.

In the years since the tocopherols were identified as vitamin E, the material sold for research and for use as a nutritional supplement has changed drastically several times, even when it has been given a specific chemical identity, such as mixed tocopherols or d-alpha tocopherol. Variations in viscosity and color, caused by changes in the impurities, have undoubtedly influenced its biological effects, but the ideology about its antioxidant value has kept researchers from finding out what a particular batch of it really is and what it really does.

"We compared the effect of a mixed tocopherol preparation with that of alpha-tocopherol alone on superoxide dismutase (SOD) activity and iNOS expression in cultured myocytes exposed to H-R." "Both tocopherol preparations attenuated cell injury. . . .” “However, mixed-tocopherol preparation was much superior to alpha-tocopherol in terms of myocyte protection. . . .” “Lack of efficacy of commercial tocopherol preparations in clinical trials may reflect absence of gamma- and delta-tocopherols."

Chen H, Li D, Saldeen T, Romeo F, Mehta JL,Biochem Biophys Res Commun 2002 "Mixed tocopherol preparation is superior to alpha-tocopherol alone against hypoxia-reoxygenation injury."

Keeping our diet as free as possible of the polyunsaturated fats, to create something like the "deficiency" state that is so protective (against cancer, trauma, poison, shock, inflammation, infection, etc.) in the animal experiments, seems preferable to trying to saturate ourselves with antioxidants, considering the imperfectly defined nature of the vitamin E products, and the known toxicity of many of the other antioxidants on the market.


Sounds like the bacteria Vit. E in our digestive system is a better source.
 

Travis

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Per Ray- A possible mitochondrial site for toxicity: In 1971 I was trying to combine some of the ideas of Albert Szent-Gyorgyi, Otto Warburg, W. F. Koch, and L. C. Strong. I was interested in the role of ubiquinone in mitochondrial respiration. In one experiment, I was using paper chromatography to compare oils that I had extracted from liver with vitamin E and with commercially purified ubiquinone. Besides using the pure substances, I decided to combine vitamin E with ubiquinone for another test spot. As soon as I combined the two oils, their amber and orange colors turned to an inky, greenish black color. I tested both bacterial and mammalian ubiquinone, and benzoquinone, and they all produced similar colors with vitamin E. When I ran the solvent up the paper, the vitamin E and the ubiquinone traveled at slightly different speeds. The black spot, containing the mixture, also moved, but each substance moved at its own speed, and as the materials separated, their original lighter colors reappeared. Charge-transfer bonds, which characteristically produce dark colors, are very weak bonds. I think this must have been that kind of bond. Years later, I tried to repeat the experiment, using "ubiquinone" from various capsules that were sold for medical use. Instead of the waxy yellow-orange material I had used before, these capsules contained a liquid oil with a somewhat yellow color. Very likely, the ubiquinone was dissolved in vegetable oil. At the time, I was puzzled that the color reaction didn't occur, but later I realized that a solvent containing double bonds (e.g., soy oil or other oil containing PUFA) would very likely prevent the close association between vitamin E and ubiquinone which is necessary for charge-transfer to occur. Since I think Koch and Szent-Gyorgyi were right in believing that electronic activation is the most important feature of the living state, I think the very specific electronic interaction between vitamin E and ubiquinone must play an important role in the respiratory function of ubiquinone. Ubiquinone is known to be a part of the electron transport chain which can leak electrons, so this might be one of the ways in which vitamin E can prevent the formation of toxic free-radicals. If it can prevent the "leakage" of electrons, then this in itself would improve respiratory efficiency. If unsaturated oils interfere with this very specific but delicate bond, then this could explain, at least partly, their toxicity for mitochondria. ["Electron leak" reference: B. Halliwell, in Age Pigments (R. S. Sohal, ed.), pp. 1-62, Elsevier, Amsterdam, 1981.]


Still having a hard time believing any Vit. E in a yellow color capsule is beneficial.
Albert Szent-Györgyi writes a lot about charge transfer complexes, and I think the book in which he does so the most has a free online .pdf edition.. .

Szent-Györgyi, Albert. "Bioenergetics." Academic Press (1957)

He defines a charge transfer as a one-electron transfer, differentiating it from the more common two-electron oxidation–reductions (±2e⁻).
 

Mossy

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I have started to test this one but I asked the manufacturer to verify what it is...

2018-03-19_13-17-08.png
It will be interesting to hear their response, because according to the chart @schultz posted, wheat germ oil derived vitamin e should be more a-tocopherol dominant--just like Tocovit. To note, I'm not dogging any of these oils, just curious how they can call out the y-tocopherols on the label--which to me suggests it's a major component.
 

Aleeri

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More from Peat-

Besides antagonizing some of the end effects of the toxic fatty acids, vitamin E inhibits lipolysis, lowering the concentration of free fatty acids (the opposite of estrogen’s effect), and it also binds to, and inactivates, free fatty acids. The long saturated carbon chain is very important for its full functioning, and this saturated chain might allow it to serve as a substitute for the omega -9 fats, from which the Mead acid is formed. The unsaturated tocotrienols have hardly been tested for the spectrum of true vitamin E activity, and animal studies have suggested that it may be toxic, since it caused liver enlargement.

I think this stuff from Peat is outdated. Tocotrienols and palm fruit seems to be looking much better now on paper: http://peatarian.com/31268/peat-critical-review-series-tocotrienols-really-benefits

Also here is another quote from Ray from above post (not sure when he said this):

This is what Peat has to say about palm oil:

"In a comparison of many kinds of oil, including linseed oil, olive oil, whale oil, etc., palm oil appeared to be the most protective. The same researcher [32] more recently studied palm oil's antithrombotic effect, in relation to platelet aggregation. It was found that platelet aggregation was enhanced by sunflowerseed oil, but that palm oil tended to decrease it."

"Although I don't recommend "palm oil" as a food, because I think it is less stable than coconut oil, some studies show that it contains valuable nutrients. For example, it contains antioxidants similar to vitamin E, which lowers both LDL cholesterol and a platelet clotting factor. [B. A. Bradlow, University of Illinois, Chicago; Science News 139, 268, 1991.] Coconut oil and other tropical oils also contain some hormones that are related to pregnenolone or progesterone."



Some studies from above thread:

Red palm oil vs. other oils

In hamsters, red palm oil lead to significantly less aortic cholesterol deposition and lower plasma lipid hydroperoxide values than coconut oil
Different palm oil preparations reduce plasma cholesterol concentrations and aortic cholesterol accumulation compared to coconut oil in hypercholes... - PubMed - NCBI

In rats, palm oil caused significantly lower serum lipid peroxides than butterfat.
Effects of dietary palm oil on serum lipid peroxidation, antithrombin III, plasma cyclic AMP, and platelet aggregation - ScienceDirect

In nonhuman primates, palm olein oil caused significantly less artherosclerosis than sunflower oil or lard.
http://www.ncbi.nlm.nih.gov/pubmed/12492629

In mice, palm oil ingestion during a high-fat diet caused significantly lower endotoxinemia than sunflower oil, rapeseed oil, and (non-significantly) milk fat.
http://www.ncbi.nlm.nih.gov/pubmed/22094473

Red palm oil vs. refined/heated palm oils

In rabbits, red palm oil caused significantly less artherosclerosis than refined palm oil
http://www.nrjournal.com/article/S0271-5317(00)00166-4/abstract

In rats, fresh palm oil lead to significantly less atherosclerotic plaques than palm oil that was reheated several times
http://www.ncbi.nlm.nih.gov/pubmed/23320039



The only thing I am worried about is the beta-carotene content in Palm fruit when supplemented for Vitamin E, as the content tends to get high. On the palm fruit supplement I have, it says mixed carotenoids 30mg (3,960mcg Vitamin A 440% RDA)

Cause for concern?
 
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It will be interesting to hear their response, because according to the chart @schultz posted, wheat germ oil derived vitamin e should be more a-tocopherol dominant--just like Tocovit. To note, I'm not dogging any of these oils, just curious how they can call out the y-tocopherols on the label--which to me suggests it's a major component.

It’s alpha. They admitted making a mistake on their label.
 

Mossy

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It’s alpha. They admitted making a mistake on their label.
Oh wow--what a mistake. o_O Could be misleading, to some degree. But, I guess you could argue it does have y-tocopherol in it.
 
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Obi-wan

Obi-wan

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http://www.jarrow.com/product/221/Gamma_E

Other Ingredients
Softgel consists of gelatin, glycerin, purified water and organic caramel.

No wheat, no gluten, no dairy, no egg, no fish/shellfish, no peanuts/tree nuts.


This could be the one!
 
J

jb116

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http://www.jarrow.com/product/221/Gamma_E

Other Ingredients
Softgel consists of gelatin, glycerin, purified water and organic caramel.

No wheat, no gluten, no dairy, no egg, no fish/shellfish, no peanuts/tree nuts.


This could be the one!
I did find this info on some other retailers who carry it;
"Other Ingredients Soybean oil. Softgel consists of gelatin, glycerin and water. Carob and caramel added as a light barrier. Contains Soy"
 
B

Braveheart

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I did find this info on some other retailers who carry it;
"Other Ingredients Soybean oil. Softgel consists of gelatin, glycerin and water. Carob and caramel added as a light barrier. Contains Soy"
Supplement Facts
Serving Size: 1 Softgel
Servings per Container: 120

Amount Per Serving % Daily Value

Vitamin E (d-alpha tocopherol) 50 IU 170%

Mixed Tocopherol Complex 500 mg *

Gamma Tocopherol 300 mg *

*Daily value not established.
Other Ingredients: Soybean oil, softgel consists of gelatin, glycerin, water, caramel and carob.
 
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Obi-wan

Obi-wan

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Again with the Soybean oil. I am already staring at various Vit. E bottles every day and they are saying don't take me...
 

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