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TocoVit - Liquid Vitamin E From Wheat Germ Oil

  1. Wow, amazing! Thanks so much for reporting.
     
  2. Sorry if this has been answered somewhere else in the thread, but why do you think there's such a difference between this E and the rest? Seeing as the newer formulation only contains the waxes alongside the E, could it be chalked up to this? Or just the superior quality?
     
  3. I don't know for sure, but this formulation is high-alpha mixed tocopherols and most other products on the market are high-gamma. The alpha tocopherol seems to be better at estrogen antagonism while gamma tocopherol seems better as scavenger of NO and other reactive nitrogen species. So, for something like gyno I would expect the alpha tocopherol to work better. The policosanols also have effects, usually by opposing PUFA.
     
  4. @haidut Have you tried reacting the new formula with ubiquinone to see if it produces a black color?

     
  5. Yes, it does. And it produces black color when mixed with vitamin K and/or emodin too, which is expected since K2/emodin are quinones.
     
  6. Awesome!
     
  7. Is there a limit to how much one can take in a day?

    Also besides pufa inactivation and estrogen lowering, what are the benefits of Vit E?
     
  8. Ok, so I know the issue of vitamin K and Vitamin E interacting in the bloodstream has been discussed many times on the forum. There should be at least 6 hours between using Vitamin K and Vitamin E to avoid having them in the bloodstream at the same time.

    But what about other quinones? Is it ok to use vitamin E and Lapodin? Or Vitamin E with a tetracycline antibiotic? These are quinones like vitamin K so do they also negatively interact with vitamin E?
     
  9. Vitamin E in doses above 800 IU daily seems to delete vitamin K and increase risk of bleeding. It may also irritate the gut in some people, especially in higher doses.
     
  10. As I mentioned to you in a PM, all quinones likely have this interaction effect. I have tried with vitamin K and emodin and both turn the vitamin E solution pitch black when mixed, similar to the experiment with CoQ10 Peta mentioned in one of his articles.
     
  11. Thanks. I also read it may flip over into an oxidant at doses above 1,100 IU.
    It is more effective than vitamin A or K, or iodine or selenium for lowering estrogen, from my use
    I will have to see how it feels when I'm not estrogen excessive (which I'm using it to treat but I want to know what effects it gives me in a healthy state)
     
  12. When I click the link on the site it brings me to this thread, how do I purchase?
     
  13. I think it says add to cart option
     
  14. Sorry if this has been answered already, but what is the absorption rate through skin @haidut ? I tried a different Vit E and it had irritated my gut.

    Also any idea how far apart do Vit K and E need to be taken? I take A,D,K during breakfast and was thinking of taking B vitamins and E after lunch
     
  15. Peat says about 30%-35% absorption of vitamin E/MCT combinations. I would firs take the vitamin K as it has relatively short half life and then 2-3 hours later the vitamin E.
     
  16. 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.
     
  17. Do you know that absorption percentage for oral use?

    And about the timing, do you think it is a good strategy to take vitamin K with breakfast, and vitamin A, D and E with lunch?
     
  18. Timing should not matter as long as it is a few hours before/after the vitamin K. Probably better to use K/D first then a few hours later to use the E/A. Oral absorption should be close to 100%.
     
  19. This is interesting. :): Any update from the Tocovit (vs Magnoil)-only approach?
     
  20. This is interesting. :): Any update from the Tocovit (vs Magnoil)-only approach?
     
  21. 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.
     
  22. 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.
     
  23. 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."
     
  24. 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)
     
  25. 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.
     
  26. 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:
    The numbers are the references located at the end of each chapter.


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

    upload_2019-1-15_14-39-8.png
    upload_2019-1-15_14-40-24.png
    upload_2019-1-15_14-41-26.png
    upload_2019-1-15_14-42-49.png
    upload_2019-1-15_14-46-4.png

    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.
     
  27. Did you take it orally?
     
  28. 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
     
  29. So what are these higher concentrations?
     
  30. 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.
     
  31. Lately, I am reacting poorly to any vitamin E supplement orally or topically.
     
  32. 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?
     
  33. 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:

    upload_2019-1-28_21-17-10.png upload_2019-1-28_21-17-15.png
     
  34. 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).

     
  35. 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!
     
  36. 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)

    upload_2019-1-29_13-37-56.png
    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.
     
  37. 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.
     
  38. 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.'"

    Is it the refined or the previous version?
     
  39. This is interesting, it kinda makes sense. Too much salt causes almost the same feeling.

    I still have the previous version.
     
  40. This is the breakdown for the latest batch of the raw material we got:

    alpha-tocopherol = ~53.8%
    beta-tocopherol = ~18.2%
    gamma-tocopherol = ~22.5%
    delta-tocopherol = ~5.4%

    As far as imbalance, I have not see evidence for that. People in South and Eastern Europe consume food with tocopherols heavily favoring the alpha isomer and so far there have not been any studies showing this creates some kind of a health problem. People in Asia and some African countries consume more gamma-heavy foods and there has not been a reported issue with that either.
    The point is that the original studies from the early 20th century were all done with mixed tocopherols from wheat germ oil and that one is alpha-heavy. That is the point of Tocovit - to replicate that product. If somebody is concerned about getting more gamma they can always get something like Unique-E or another mixed tocopherol brand and supplement. The vast majority of mixed tocopherols on the market these days are sourced from soy and as such heavily favor the gamma isomer.
     
  41. Yeah, I can confirm that there is no more smell in the current version of TocoVit. As far as taste, it should not really have any pungent taste like the previous one and most people say is has hints of butter but not much else.
     
  42. Vitamin A also plays a role in sun protection via skin though (in that it gets "used up" by sun) - UV Radiation Induces Vitamin A Deficiency In Skin

    I think vitamin C does, too. While vitamin some viamin E intake is clearly necessary to tolerate sunshine, I'm convinced there's a drastic and incomparable anti-inflammatory/antioxidant effect from sunshine. Maybe UVB is simply an "activator"?

    Thanks.

    I find cultural-geographics trends to be a really important source of understanding and reflection.

    Like with Southern Europe, caucasian and latino cultures in sun rich environments seem to favour alpha tocopherol rich foods in larger quantities, where as caucasians in Northern Europe tend to favour saturated fat sources (with the addition of omega 3 from fatty fish) and have a heavy skew towards flavanol consumption as an antioxidant (via tea, chocolate, berries, veg) - this is pretty consistent throughout Northern and Central Europe.

    I think flavanols can act as a vitamin E / antioxidant surrogate, and perhaps sunshine can help deal with PUFA oxidation in some way. These correlations always work both ways, too - perhaps in sun rich environments, for caucasians, alpha tocopherol rich sources of vitamin E (PUFAs!) become a necessity to benefit from sunshine and therefore thrive. Conversely, such a high alpha tocopherol consumption WITHOUT sunshine might have adverse effect (hence to be careful with supplementaiton).

    I understand it's sacrilege to say that here but I think intuitive cultural trends are one of our best guides!
     
  43. I don't think it is sacrilege at all. Perceive, think, act rules the day and if your intuition and experience say a specific culture has good food habits then that should be the guiding force unless serious experiential (first-hand) evidence to the contrary accumulates.
     
  44. :thumbsup:
     
  45. I get an off feeling from low dose daily kuinone, a kind of emotionless feeling (though I don't get it using a high dose just once or twice a week)

    Would it be a good idea to put vit E on the testes along with pansterone to prevent aromatization?
     
  46. I don't think there is a need to put everything on the scrotum. Only steroids have proven benefit when placed there. Topical application anywhere on the body should be good enough.
     
  47. Peter Surai | Researching the Gates
    Antioxidant-Prooxidant Balance in the Intestine: Food for Thought

    "Vitamin E, the most effective natural free radical scavenger identified to date, is the main chain breaking antioxidant in the cell. However! Hydroperoxides, produced in the reaction of vitamin E with the peroxyl radical, are still toxic and if not removed, impair membrane structure and functions (Gutteridge and Halliwell, 1990). As shown above, lipid hydroperoxides are not stable and in the presence of transition metal ions can decompose producing new free radicals and cytotoxic aldehydes (Diplock, 1994). Therefore hydroperoxides have to be removed from the cell in the same way as H2O2, but CAT is not able to react with these radicals and Se-dependent GSH-Px can deal with these potentially toxic compounds converting them into non-reactive products (Brigelius-Flohe, 1999) as follows:

    ROOH + 2GSH >> GSH-Px >> ROH (non-toxic) + H2O + GSSG
    Thus, vitamin E performs only half the job in preventing lipid peroxidation by scavenging free radicals and forming hydroperoxides. The second part of this important process of antioxidant defence is due to Se-GSH-Px."

    upload_2019-1-31_19-45-59.png

    "This figure demonstrates a connection of antioxidant defence to the general body metabolism (the pentose phosphate cycle is the major producer of reducing equivalents in the form of NADPH) and shows involvement of other nutrients in this process. For example, dietary protein is a source of essential amino acids for glutathione synthesis, riboflavin is an essential part of glutathione reductase, niacin is a part of NADPH and Se is an integral part of thioredoxin reductase. At the same time thiamine is required for transketolase in the pentose phosphate pathway."

    "Thus, a major finding in recent years is the possibility of direct or indirect vitamin E recycling from its oxidised radical form by means of ascorbate (Chan et al., 1991; Chan, 1993), glutathione (Niki et al., 1982; Chan, 1993), cysteine (Motoyama et al., 1989), ubiquinols (Freisleben and Packer, 1993; Chan, 1993), lipoic acid (Packer, 1998), estrogens (Mukai et al., 1990), carotenoids (Palozza and Krinsky, 1992; Bohm et al., 1997) and potentially quercetin and catechins (Pietta, 2000; raiser, 2019), anthocyanins (Frank et al., 2002) and rosemary extracts (Madsen et al., 1997). Enzymatic regeneration of a-tocopherol has been also described (Maguire et al., 1989; Kagan et al., 1998). The rate of reduction of phenoxyl radical in the membrane decreased in the order of ascorbic acid>cysteine>glutathione (Niki, 1996). The rate of regeneration, or recycling, of the vitamin E radicals that form during their antioxidant action may affect both its efficiency in antioxidant action and its lifetime in biological systems and the greater recycling activity is associated with increased efficiency of inhibition of lipid peroxidation (Packer, 1995). Whether all these regeneration reactions take place in vivo await investigation. Due to incomplete regeneration (the efficiency of recycling is usually less than 100%) in biological systems, the antioxidants have to be obtained from the diet (e.g. vitamin E and carotenoids) or synthesised in the tissues (glutathione)."

    "Therefore the antioxidant protection in the cell depends not only on vitamin E concentration and location, but also relies on the effective recycling. Indeed, if the recycling is effective then even low vitamin E concentrations are able to maintain high antioxidant protection in physiological conditions. For example, this could be demonstrated using chicken brain as a model system. Indeed, our data (Surai, 2002) indicate that the brain is characterised by extremely high concentrations of long chain polyunsaturated fatty acids predisposing this tissue to lipid peroxidation. Furthermore, brain contains much lower levels of vitamin E than other body tissues. However, in fresh chicken brain, levels of products of lipid peroxidation are very low, which could be a reflection of an effective vitamin E recycling by ascorbic acid which is present in this tissue in comparatively high concentrations. Antioxidant recycling is the most important element in understanding mechanisms involved in antioxidant protection against oxidative stress. Therefore, regeneration, or recycling, of the vitamin E radicals may affect both its antioxidant efficiency and its lifetime in biological systems."


    "It was observed that the generation and accumulation of NO from typical nitrite concentrations found in biological tissues increases 100-fold when the pH falls from 7.4 to 5.5 (Zweier et al., 1999). Therefore nitrate and nitrite can generate NO* radical by either direct disproportionation or reduction under the acidic and highly reduced conditions (Chow and Hong, 2002). More importantly, NO* can be a source of another reactive free radical peroxynitrite (ONOO-), which is 1000 times more oxidizing than H2O2 and has half-life in solution about 1–2 seconds (Van Dyke, 1997). It is well accepted that peroxynitrite is a potent cytotoxic agent (Pryor and Squadrito, 1995; Squadrito and Pryor, 1998). Peroxynitrite can also affect antioxidant system by changing activities of antioxidant enzymes. In fact peroxynitrite has been shown to inhibit the activities of catalase (Keng et al., 2000), GSH-Px (Padmaja et al., 1998) and promote lipid peroxidation (Shi et al., 1999). Moreover, it appears that ONOO can oxidize a variety of essential molecules (e.g., sulfhydryls, thiols, ascorbate, proteins, DNA) and trigger injurious processes, including lipid peroxidation (Patel et al., 1999, Hogg and Kalynaraman, 1999). On the other hand, peroxynitrite may be decomposed forming highly reactive hydroxyl radical (*OH) and nitrogen dioxide (Beckman et al., 1990; Augusto et al., 1994)."

    "At least 25% of world’s grain production is contaminated with mycotoxins, which are a worldwide problem [and another source of oxidative stress] (Fink- Gremmels, 1999). For example, aflatoxins are considered to be unavoidable contaminants of food, since they cannot be prevented or eliminated by current agricultural practice (Peraica and Domijan, 2001). The intake of aflatoxin M1 from milk was calculated to vary from 0.1 ng/person/day in Africa up to 12 ng/person/day in Far Eastern countries (Creppy, 2002)."

    "It is necessary to stress that the nutrient requirement to maintain a highly active immune system in the digestive tract could be quite high. In fact different sources of injury to the intestinal mucosa (nutritional, infectious or allergic) act via a common mechanism of cell-mediated immune damage and nutrient repletion is required for restoration of immune function (Cunningham-Rundles, 2001)."
     
  48. I am tempted to order the new version now. Do you take it only orally? What am I going to do with the 6 whole bottles of the old version? :arghh:
     
  49. That sounds like anemia. Vit E is an extremely powerful iron antagonist, and has personally caused anemia for me. My symptoms were vertigo, mentally zoning out, and feeling short of breath in the middle of speaking. If that sounds like you, you should back off using it and maybe get some blood work. It was no joke, and took awhile to ameliorate.
     
  50. I've tried on skin just for the sake of confirming that it doesn't irritate anymore, so I never went over the boards with dosages.

    Even though it's an inferior product, perhaps there are people who weren't affected by the change and might be interested in buying for a lower price.
    My experience has some similaritaies to yours. I initially suspected that, but vitamin E has been shown with consistency to improve various forms of anemia.

    I don't think it can deplete iron in a matter of days, we pimps tend to have hundreds of milligrams stored; and if it can, it should not be correctable in such a short frames times. A change in blood dynamics affecting how iron is being delivered to tissues is possible, but it usually improves this aspect as well, and I find it less likely than many other factors that might be responsible, like an excess of antioxidant disrupting cell signalling, imbalances between them, a detrimental interference with ubiquinone, modification of local vitamin K metabolism, and so on.

    - Studies on interactions of vitamin E with thiamine, niacin and vitamin B12

    "DL-a-tocopheryl acetate at a dose of 100 mg--three times daily for a period of 15 days."

    "Estimation of the erythrocyte enzymes aspartate aminotransferase (EC 2.6.1.1) (EAST) for pyridoxine, glutathione reductase (EC 1.6.4.2) (EGR) for riboflavin and transketolase (EC 2.2.1.1) (ETK) for thiamine have been shown to reflect the nutritional status of these vitamins, respectively, fairly well [6]."

    upload_2019-2-1_19-59-34.png

    "The observation of a reduction in basal and stimulated activities of EAST following administration of vitamin E is interesting. However, the effect was transitory as the levels came back to normal by the 30th day. Although there is not much information on the day-to-day variations in the enzyme activity, the reduction appears to be an effect of vitamin E administration and not a physiological variation. Since there was a reduction in both basal and stimulated activities, the activity coefficient remained unaltered. Such a situation can occur when there is either a reduction in apoenzyme content or there is inhibition of the binding of the cofactor to the apoenzyme. The latter possibility is probably not true as the enzyme activities returned back to normal levels in spite of continued treatment. A transient reduction in the apoenzyme content, however, appears to be a possibility."

    "Vitamin E has been shown to have some effect on protein synthesis [23]. Since the amount of vitamin E administered is rather high, some transient effect on protein synthesis in reticulocytes cannot be ruled out."

    "To assess the nutritional status of vitamins as judged by the erythrocyte enzyme activities, activity coefficient values are considered to be the best index. Since there was no change in activity coefficient because of a simultaneous decrease in both basal and stimulated activities, we are not in a position to comment upon the effect of vitamin E administration on nutritional status of pyridoxine and riboflavin."​

    - Interactions between ubiquinones and vitamins in membranes and cells
     
  51. Very interesting! Still though, it was all the classic signs of anemia. For me it makes sense that it was anemia, since all the things I was doing at the time were about antagonizing iron (coffee drinking with iron rich meals, no vit C foods around iron, taking vit E everyday, working out, eating a high vit C diet, getting lots of uvb, lots of Mg in diet etc.) and my experiences are pretty identical to the peeps online who end up having to use liquid iron supps to get healthy again (usually distance runners). It was sucky, I thought I was becoming hypotensive but my vitals were fine. Interesting about the B's, I think if we can conclude anything vit E is not a toy lol.
     
  52. A boombox is not a toy either. I believe in the you for knowing the feeling very well. There are various publications from doctors reporting mysterious fatigue in patients after vitamin E supplementation if you search for it, but it's controversial. It seems to me a matter of improper individualized dosing (can't speak for topical use).

    - Thrombophlebitis Associated With Vitamin E Therapy - With a Commentary on Other Medical Side Effects

    "I have encountered 50 patients with clinical thrombophlebitis involving the lower extremities, with or without associated edema and pulmonary embolism, in whom longstanding self-medication with large amounts of vitamin E appeared to be a significant factor. The majority improved following cessation of vitamin E.

    In view of the epidemic nature of thrombophlebitis and deep vein thrombosis in the United States, the presumed innocuousness of vitamin E therapy requires reevaluation.

    Other clinical side effects also have been noted in patients receiving large doses of vitamin E. They include breast tenderness, elevation of blood pressure, a fatigue symdrome, myopathy, intestinal cramps, urticaria, and the possible aggravation of diabetes mellitus.

    The influence of concomitant metabolic, endocrine, and cardiovascular disorders on the thrombogenic potential of vitamin E is raised, and several possible mechanisms conducive to thrombophlebitis are reviewed."​

    "Side Effects

    As with other pharmacologically active drugs, there are side effects associated with vitamin E therapy.
    1. The most significant side effect to which reference previously has been made is a transient elevation of blood pressure.[3]
    2. A severe fatigue syndrome was attributed to "hypervitaminosis" by Cohen,[14] who regarded this condition to be a more common cause of fatigue than anemia and hypothyroidism.
    3. Diarrhea and intestinal cramps have been reported in patients taking large doses of vitamin E.
    4. A mild myopathy has been ascribed to vitamin E. Elevated serum creatinine kinase levels accompanied by creatinuria were found in healthy young men given 800 IU daily of d-alpha tocopheryl acetate in a double-blind study by Briggs.[15] These changes normalized 7 days after the treatment was stopped, and were attributed to possible skeletal muscle damage.
    5. I have encountered recurrent urticaria that was conclusively demonstrated to be due to vitamin E in a patient receiving 400 IU daily.
    6. I have suspected that vitamin E aggravates diabetes mellitus, albeit infrequently. The following patient is an example:
      • A 52-year-old diabetic male was evaluated for recently uncontrolled diabetes while on oral hypoglycemic drugs. He was shifted to insulin, and repeatedly maintained at normoglycemic levels with 20 units of Lente insulin daily. His fasting blood glucose concentration then unexpectedly rose from 102 and 104 mg/100 ml to 152 mg/100 ml. The patient recalled that he took a vitamin E capsule the previous day (but not the day of the test). After stopping the vitamin E, his glucose concentrations were 100 and 105 mg/ 100 ml. He then volunteered that his previous good control while on tolbutamide abruptly changed following self-medication with vitamin E-although this association was gleaned only in retrospect. Thereafter, his blood glucose concentrations rose to high levels, requiring hospitalization.
    7. Caralis[16] was unable to demonstrate significant symptomatic or functional improvement of angina pectoris among 48 patients who took 1600 units of d-alpha tocopherol daily for 6 months, compared with placebo administration for 6 months. The patients’ diaries showed that the average number of anginal attacks per week, however, actually increased during the tocopherol months.
    There are other ramifications of interference with intermediary metabolism by vitamin E. McMasters and associates[17] reported both a relative increase in the adipose tissue tocopherol levels of diabetics following oral supplementation with tocopherol, and a more rapid rate of depletion. They also noted higher adipose tissue levels of tocopherol during and following supplementation in response to oral hypoglycemic medication. For example, the average tocopherol level while on tolbutamide was twice that of the group without medication, suggesting an influence on the absorption and retention of tocopherol. Bensley and associates[18] could not demonstrate improvement of diabetes with supplementary tocopherol, even though plasma tocopherol levels were doubled.

    The frequency of metabolic, cardiovascular, and endocrine disorders in this series of patients is germane. They included diabetes mellitus, reactive hypoglycemia (with or without decreased glucose tolerance), hypertriglyceridemia, hypercholesterolemia, subacute or chronic anicteric hepatic dysfunction (generally diagnosed on the basis of considerable Cardiogreen retention), hypothyroidism, and hyperuricemia. In view of the known tendency to small vessel disease, platelet aggregation, and a thrombotic diathesis in diabetes, hyperlipidemia, and hyperuricemia, the possibility of a potentiated thrombogenic action by vitamin E appears likely. The same applies to preceding or concomitant estrogen and contraceptive therapy."
    "Possible Modes of Action

    The following are possible modes of action whereby vitamin E may cause or contribute to thrombogenesis. Many of these effects of vitamin E on cellular biochemistry, biosynthetic regulation, and hematopoiesis were reviewed in the Proceedings of the International Conference on Vitamin E.[2]
    1. An increase of circulating triglycerides, cholesterol, and perhaps other lipids.[22]
    2. An increase of hepatic lipid and cholesterol.[23]
    3. Other alterations of intermediary metabolism mentioned in the preceding discussion.
    4. An enhanced immune response.[23-25] Harman and colleagues[28] provided evidence that vitamin E can enhance the humoral immune response in aging mice. It has been demonstrated that older mice have only 10% of the humoral capacity (mediated by B lymphocytes) of younger animals,[29] perhaps as a result of endogenous free radical reactions. These observations assume even greater importance in view of the large number of older individuals who are taking vitamin E preparations for their alleged benefit in cardiovascular and other degenerative diseases.
    5. Alterations of hormone metabolism, especially through the action of vitamin E on the microsomal enzyme drug hydroxylating complex in the liver.[21]
    6. The mobilization and increase of platelets.[3]
    7. The induction of abnormal erythrocytes and vascular membrane lipid peroxidation-the antioxidant effect of tocopherols preserving reduced glutathione stability through the maintenance of sulfhydryl bonds.[1,2,23]
    8. Increased erythropoiesis (as demonstrated in the monkey) stemming in part from an enhancement of the androgen effect by vitamin E,[27] combined with a possible decreased rate of hemolysis."
     
  53. Really insightful and relevant to my personal experience - good find(s)!

    On the topic of anthocyanins playing a role it might help explain why I find tart cherry juice to be the best tasting thing ever in the world!
     
  54. Hahahaha :lol: This is true.

    Thanks for the write up! I guess maybe the vertigo, shortness of breath could be because of E's interference of b vitamin function, but it also seemed to be worsened by high calcium food, like suddenly I became intolerant to milk and it would worsen the dizziness. That's another reason I figured it was anemia.
     
  55. Jon, the foro informed me that Blossom is online right now. This means that there's a great chance that she'll be reading this message. How nice is that?

    I have been insisting that to find the proper dose of supplements it's easier to work the way up instead of the opposite. In this approach we're supposed to feel better and better as we increase it, being clear when it plateaus or when it starts to have a detrimental effect. Contrary to this, if you start with a high dose, you run the risk of adapting to an improper condition and it will be more difficult to discern what is ideal, as we lower there will be a conflict between feeling worse and improving some aspects; with the discomfort we feel tempted to return to the accustomed dose and settle with it.

    As an example, they mentioned above that the change in pyridoxine was transient and by the time of the next measurement it normalized. The same must occur if you insist on a mistaken amount.
     
  56. - Safety of Antioxidant Vitamins

    upload_2019-2-8_19-25-24.png
    There's a brief comment on each in the document. Some are absurd, others are not.​

    Just stressing that the negative effect that I'm experiencing is not from Zeus' product, it's from a fμcking soap (!). I figured it could be useful to post these here in case some of you are getting or eventually get (mysterious) undesirable reactions. Such adhiveatoiatsies are for the most part benign in the nature, and it seems that you have to be a freak to experience them given how rare they appear to be, but they're possible.
     
  57. Waving my freak flag :hungover:
     
  58. Some questions if you don't mind:
    - How much were you taking?
    - What route?
    - After stopping it, how long did it take to return to normal?
    - Your average cupre consumption is on the lower or higher side?
    - What about choline?
    - How much vit C, vit K and proteid were you getting?

    I was suspecting that if there's one nutrient that's likely to be interfered the most based on what was posted here is copper. It can explain everything ranging from anemia and fatigue to typhoid disturbances. Perhaps a redistribution of some sort as it happens when you take a lot of vit C or through hormonal effects like estrojen (with clues from tit issues as well, for a lack of refinement). Copper is required for collagen and vascular integrity, so anything related to skin manifestations such as dermatitis but also bleedings can involve it. Lipid alterations from changes in copper adequacy is classic. It's also a more likely candidate to be depleted than iron given the frame time.

    It wouldn't be surprising if the intolerance to foods high in calcium was due to its effects on vit K.
     
  59. No indication that it worsened an iron deficiency, it actually helped in correction:

    - Role of vitamin E in iron deficiency anemia

    upload_2019-2-15_19-47-3.png

    "As to the cause of decreased serum vitamin E level in iron deficiency anemia, increased vitamin E demand in the body and insufficient intake of dietary vitamin E were considered to be major factors."

    "Increased demand for vitamin E in the body may be explained by increased consumption of vitamin E due to remarkable change of endocrine function and rapid iron turnover in iron deficient state. Vitamin E is known to have close relationship with endocrine functions, particularly with the function of sex glands.[6,7,8,9]"

    "Therefore, remarkably increased excretion of gonadotropin due to ovarian dysfunction which, as previously reported,[5] was observed in most iron deficiency anemia may bring about the increased demand for vitamin E."

    "It is known that vitamin E has reducing action on iron,[10] reducing it from ferric to ferrous iron."

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

    "The release of iron from ferritin stores requires mobilization and reduction of Fe3+. Reductases and/or reducing substances such as riboflavin (FMNH2), niacin (NADH), or vitamin C may play roles in the reduction of the iron."

    "Following this reduction of iron to release it from storage, Fe2+ is transported to the cell's plasma membrane, where it must bind to ferroportin and be reoxidized. This reoxidation of iron requires ceruloplasmin and enables it to bind to transferrin for transport in the blood to other tissues."

    upload_2019-2-15_19-47-45.png
    "Ferrokinetic studies disclosed the fact that rapid turnover of iron with frequent reduction of iron from ferric to ferrous iron occured in cases of iron deficiency anemia.[11] Accordingly demand for vitamin E was considered to increase in cases of iron deficiency anemia."

    "Increased vitamin E level following iron therapy may be explained as follows. After recovery from anemia iron turnover is known to return to normal, resulting in decreased demand for vitamin E for reduction of iron. This decreased demand for vitamin E may be considered to increase serum vitamin E level to normal rate."

    "The facts that vitamin E was effective for prevention of relapsing and for treatment of iron deficiency anemia with insufficient recovery may indicate favorable effect vitamin E on erythropoiesis in iron deficiency anemia."

    It must be something else. But regarding interference with vit C, it improved its steady level in blood (healthy people):

    - Partners In Defense, Vitamins E And C


    --
    - Vitamin E: Emerging aspects and new directions (!)

    upload_2019-2-15_19-49-37.png

    - Aldehyde Dehydrogenase
    - Molybdenum, Hard To Pronounce, Harder Still To Obtain

    :confused2 :confused2 :confused2
     
  60. The amount I took varied depending on how much PUFA I ate from day to day. I can’t remember now how I figured it out but it was something like for every 1g of PUFA ingested you need like 2mg of vit E?

    I think that usually worked out to like 10-20mg a day taken orally for me (hardly anything at all).

    For choline I mostly get mine from eggs (3-4 a day) along with leafy greens, and once I awhile some liver.

    I usually get about 1mg if K1 from cooked spinach and supplement 5mg K2 mk-4 daily.

    I usually get 400-500mg vitamin c from diet (fruit, veggies, juice)

    I also eat roughly 1g of protein per lb of body weight, though I only target to get 0.8g of protein per lb of lean mass. I just usually end up getting extra inadvertently.

    It took forever to go away. The stomach issues (nausea) went away after like 3 weeks, but the odd spacey feeling like I couldn’t focus my attention on anything and just wanted to stare off into space lasted considerably longer, like 3 months or so.

    I Don’t know? Maybe I just really didn’t need any because my diet is good, I’m lean, and exercise? Perhaps only a little bit was plenty to cause copper to drop?
     
  61. What if in your case it coated your intestines? How topical use affects you?
    What about molybdenum?

    I thought I was the only one having these kind of reactions, so thank you for sharing your experience because it has been helpful in trying to elucidate this issue. The effect on me is quite harsh, but in my case I suspect it induces and resolves faster, not sure.
     
  62. Hey no prob homie :) happy to help.

    I wouldn’t assume my intake of molybdenum was very high. I never ate beans or lentils so my only source of it would have been eggs and spinach, both of which I don’t think are especially high in molybdenum.
     
  63. But now that I think of it the dose was modest.

    Vit K adsorption can be compromised even during normal digestion:
    - What Are Your Best Fat Soluble Vitamins Combinations From Personal Experience?

    If I'm not wrong it can also get in the way of carotene uptake. And if you were using vit K on skin, I guess it can still be detrimental if not much is able to reach the liver.

    But the coating seems a likely possibility to consider. How it affects you when applied on skin?
     
  64. I wasnt using vit k on skin. I take all my supps orally, and have been using Carlson’s mk-4 (but they recently discontinued it :arghh:)

    Ive never tried E on skin nor vitamin K2.
     
  65. Don't you drink milk Jon?
     
  66. Yes I love it lol but during this I’d phase I had to cease drinking it. I’ve been able to take it back up though.
     
  67. @haidut
    I have a pure DHEA powder and a pure pregnenolone powder that I want to create a topical supplement with, would it be feasible to use your tocovit as a base? If so, how should I heat it up without destroying the supp or leaching plastic so I can mix the two?

    I have been using progesterone in vit E with great success so I’d like to optimize a combination of the three hormones. I tried stressnon but I have gotten some uncomfortable side effects from it that I didnt get from oral pregnenolone powder. Due to this I’m thinking it may be one of the solvents so I’d like to try it in vit E, especislly considering my success with the progesterone in E. I have already been using tocovit for a few years without issue so I thought it’d be a good base. I wanted to use it for the DHEA as a solo supplement so I can tease out the individual effects of the DHEA and the Preg. I’m going to use pansterone with MCT and tocopherol to see the combined effect.
     
  68. You would have to pour some of the vitamin E from the plastic bottle into a container that is hear resistant. Then, after dissolving the steroids you have to wait until it cools off and then pour back. But it should work, I have used TocoVit as a base for CortiNon before so I don't see why it won't work for your experiment as well.
     
  69. Thanks for your response haidut. I’ll keep you posted on the experimentation.