TocoVit - Liquid Vitamin E From Wheat Germ Oil

[milk_lover]

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?

This is interesting, it kinda makes sense. Too much salt causes almost the same feeling.

I still have the previous version.

 

[Amazoniac]

I still have the previous version.

It can explain your experience.
". Doing It Every Day(soap) Is An "Endocrine Disrupter. "

The refined version shouldn't have those issues, it's worth a try. The processing made it excellent.

 

[haidut]

@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?

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.

 

[haidut]

It can explain your experience.
". Doing It Every Day(soap) Is An "Endocrine Disrupter. "

The refined version shouldn't have those issues, it's worth a try. The processing made it excellent.

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.

 

[sunraiser]

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)

View attachment 12014
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.

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"?

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.

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!

 

[haidut]

I understand it's sacrilege to say that here but I think intuitive cultural trends are one of our best guides!

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.

 

[Braveheart]

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.

 

[Gone Peating]

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?

 

[haidut]

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?

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.

 

[Amazoniac]

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."

"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)."

 

[milk_lover]

It can explain your experience.
". Doing It Every Day(soap) Is An "Endocrine Disrupter. "

The refined version shouldn't have those issues, it's worth a try. The processing made it excellent.

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?

 

[Jon]

Been trying the new vitamin E for a few days now. I take 4 drops orally with food, maybe an hour later my skin and body feel really warm. The first day I took a dose of 12 drops (orally) later on had a "vertigo" feeling. Not sure what it was due to, but could be better oxygenation to the brain which is great!

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.

 

[Amazoniac]

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?

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.

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.

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]."

"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

 

[Jon]

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]."

View attachment 12047

"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

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.

 

[Amazoniac]

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.

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."

 

[sunraiser]

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."

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"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)."

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!

 

[Jon]

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."

Hahahaha 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.

 

[Amazoniac]

Hahahaha 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.

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.

 

[Amazoniac]

- Safety of Antioxidant Vitamins

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.

 

[Jon]

- Safety of Antioxidant Vitamins

View attachment 12146
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.

Waving my freak flag