How Much Vitamin E In A Day? (Dosage Question)

[Logan-]

How much vitamin E do you take in a day? Do you prefer taking it daily or weekly? What brand do you use? Should vitamin E be taken long term or short term?

 

[meatbag]

I liked the vitamin e I tried from lotion crafter and tocovit seemed really good. I think there's a quote from ray saying to not use more than 100 i.u. daily if using it for a while but I can't find it so please don't take that number too seriously but he has obviously stated to only use as much as needed and to be cautious; paying attention to temps, pulse, symptoms, etc. Also not to use at the same time as vitamin k. Here's some of the stuff posted on the wiki---

From: Ray Peat Email Exchanges - Ray Peat Forum Wiki
Vitamin E
My thesis adviser, Arnold Soderwall, did some studies showing that vitamin E extended fertility considerably. I found some of his old Sigma (chemical company) vitamin E still in the freezer, and I was working on the idea that oxidative catalysts in the liver were directly related to estrogen's effects. I would extract lipids from the liver, and use paper chromatography to separate them, and for reference points I used the vitamin E and different quinones (coenzyme Q10, Q6, and benzoquinone). I happened to mix the vitamin E with one of the quinones, and noticed that it turned almost black; all of the quinones had the same effect. Putting the mixture on the paper, the moving solvent separated the original components. Delocalized electrons absorb low energy light, causing a dark color (as in black semiconductors), and Szent-Gyorgyi had expressed wonder about what could cause the dark color of the healthy liver, a color that can't be extracted as a pigment. This experiment convinced me that vitamin E could be one of the participants in delocalizing electrons for activating proteins in the way S-G suggested. However, the technology for manufacturing vitamin E has changed greatly over the years, and I have never found anything sold as vitamin E that produces the same dark colors as that old stuff from the freezer. I don't know whether the powerfully therapeutic (anti-estrogenic, clot-clearing, anti-inflammatory, quinone-reactive) old vitamin E contained 'impurities' that were effective, or whether it's that the newer materials contain impurities that reduce their effects.

It was labeled d-alphatocopherol, but it was semi-solid, like crystallized honey.

Pure vitamin E doesn't have any toxic effects, except when it's enough to irritate the intestine, probably because of viscosity.

[Do you take vitamin E?] No, I stopped taking it, partly because of the new manufacturing methods, that were associated for several years with adding soy oil to the product.

[Do you have a preference between with high alpha or high gamma mixed tocopherols?] In similar milligram amounts, I would prefer gamma.

I think mixed tocopherols are better than just d-alpha, but with d-alpha it's good to choose one that has a high potency per volume. I have noticed that one of Unique's products seems to be mostly other oil. I think polycosanols account for some of the viscosity, so I prefer the thick ones.

If the potency of a vitamin E product is around 1000 i.u. per milliliter, the amount of soy oil isn't a concern, but if it's only about 100 i.u./ml, then there's enough oil to matter.

The lighter consistency is because less soy oil is removed from some cheaper products. They don't have to add oil, they just leave more of it in the product. But non-GMO soy is mostly produced using other herbicides and pesticides, and each pesticide has different affinities for oil or water, so oil soluble pesticides would be the main concern, and those are generally much more volatile than vitamin E, and so if they were present in the crude oil, they would end up mostly in the refined oil, rather than in the vitamin E. The thickest, darkest, vitamin E is likely to be the cleanest.

[Should one avoid taking vitamin E with a food that naturally contains iron (eg., eggs, chocolate, liver)?] Iron in those foods won't interfere.

It can still be very protective against lipid peroxidation and inflammation, but the products have been changing frequently in the last 15 years, so I think it’s good to be cautious and use minimal doses. The vitamin E from Sigma in the 1960s and early ‘70s behaved completely differently in relation to coenzyme Q10 and other quinones, than the more recent products.

 

[Jon]

The best way to figure out how much you need is to estimate how much pufa you're utilizing and storing in a day. If you get in the average 4grams of pufa a day that a less stringent Peat diet contains and are not in a calorie deficit, then you need about 8mg of E a day which translates to about 12I.U. (Since 1g of pufa tends to utilize 2mg a-tocopherol)

If you are losing weight and know that a lot of your stored bodyfat consists of pufa then the intake should probably be the amount you get from your diet and the amount of bodyfat you're losing per day. For a 500 calorie deficit (which yields 55g of fat loss a day) plus the 4grams you get from your diet daily that equates to 119mg or 177IU of E a day.

Be careful not to over do it. Too much E will cause sodium depletion and it's not fun. I screwed up by taking too much for a couple days and it left me with dizziness that took for ever to disappear upon cessation.

The best is probably @haidut 's tocovit for purity sake and for adjustability of dose. Most E on the market is full of nasty oils and delivers wayyy too much per serving which you generally cant adjust because it's in pill form. I think taking it daily is good because everyday is different and some days you need more some days you need less, though you'll only know these fluctuations by tracking your diet so there's that.

 

[Logan-]

Thanks.

 

[BigChad]

The best way to figure out how much you need is to estimate how much pufa you're utilizing and storing in a day. If you get in the average 4grams of pufa a day that a less stringent Peat diet contains and are not in a calorie deficit, then you need about 8mg of E a day which translates to about 12I.U. (Since 1g of pufa tends to utilize 2mg a-tocopherol)

If you are losing weight and know that a lot of your stored bodyfat consists of pufa then the intake should probably be the amount you get from your diet and the amount of bodyfat you're losing per day. For a 500 calorie deficit (which yields 55g of fat loss a day) plus the 4grams you get from your diet daily that equates to 119mg or 177IU of E a day.

Be careful not to over do it. Too much E will cause sodium depletion and it's not fun. I screwed up by taking too much for a couple days and it left me with dizziness that took for ever to disappear upon cessation.

The best is probably @haidut 's tocovit for purity sake and for adjustability of dose. Most E on the market is full of nasty oils and delivers wayyy too much per serving which you generally cant adjust because it's in pill form. I think taking it daily is good because everyday is different and some days you need more some days you need less, though you'll only know these fluctuations by tracking your diet so there's that.

how much E starts causing sodium depletion. Btw does vitamin E deplete anything else. like vitamin C, A, D, K, or other minerals like iron, calcium, etc?
I was thinking of doing thornes Ultimate E softgel twice a week, and nutrigolds vitamin E gold twice a week?

 

[Lokzo]

Be careful not to over do it. Too much E will cause sodium depletion and it's not fun. I screwed up by taking too much for a couple days and it left me with dizziness that took for ever to disappear upon cessation.

Oooooooh ***t!!!!

I have LOW sodium on my blood tests and low cortisol, this could explain why the Vitamin E in high amounts makes me feel dizzy! I thought it was because Vitamin E chelates Iron!

 

[Chromeo]

I take the DeltaGold Tocotrienols that comes from Annatto. 125 mg/1 daily.

I like it and feel good on it but it makes me very relaxed and ready for a nap.

 

[Tristan Loscha]

Concentrations of Vitamin E in pork-meat can reach 2.6mg per gram of fresh meat.So thats very high if we see that there is no acknowledgement of E in Meat-Foodstuff at all.Americans have a typical intake of 7mg/d,But what if we need 50mg as an absolute minimum,or 100mg?True source of VE is fresh meat and not Veggies or even Seedoils?Didnt know that the contribution can be so high,and what if we evolved to that req.?



https://www.dsm.com/content/dam/dsm/anh/en_US/documents/DSM Whitepaper_VitaminE.pdf

Spoiler: Veterinary Use of VE

The role of vitamin E in the antioxidant
system and in enhancing meat quality
G. Litta, T.K. Chung and G.M. Weber, DSM Nutritional Products
When selecting meat and meat products, the criteria buyers typically look for are color,
flavor and texture. As the most immediate sign of quality, the visual aspect is usually the
first parameter evaluated by consumers.
The origin of meat quality deterioration may come from different factors including genetics, as
well as improper practices in either pre-slaughtering or in post-slaughtering handling, storage
or cooking. However, lipid oxidation is probably the most important factor impacting the above
mentioned parameters. Vitamin E can play an important role in reducing meat deterioration
and color changes by reducing the negative effects of oxidation. This whitepaper discusses the
unique antioxidant role of vitamin E and how this supports the stability of meat, with a review of
key studies looking at the vitamin’s mode of action, supplementation requirements and efficacy.
Understanding lipid oxidation
Lipid oxidation is a commonly occurring process which causes foods, including meat, to
deteriorate and / or change in color. In meat, the process starts immediately after slaughter
when blood circulation stops and anaerobic metabolism starts.
Lipid oxidation is catalyzed by the presence of free radicals. These are chemical entities
with one or more free electrons which are derived from oxygen, nitrogen, sulfur and chloride.
Hydroxide and nitrogen dioxide are among the most abundant free radicals and are often referred
as ‘Reactive Oxygen Species’ (ROS) or ‘Reactive Nitrogen Species’ (RNS). Hydrogen peroxide is
not a free radical but is also very detrimental to DNA.
Reactive species are physiological products of the metabolism, displaying fundamental cellular
level functions when found in low concentration (e.g. in the immune system for the activation
of phagocytes). When their concentration exceeds a certain threshold, these species become
harmful to macromolecules such as lipids, proteins and DNA. Factors other than free radicals,
which can also promote lipid oxidation, include the presence of metals like iron and copper,
as well as compounds such as myoglobin and hemoglobin.
Importantly, lipid oxidation is an autocatalytic process. The products of oxidation catalyze
further oxidations, resulting in a chain reaction. Once this cyclical process starts, the reaction
rate rapidly increases.
Unsaturated fats – in particular those with a large number of double bonds – are extremely prone
to oxidation. Cell membranes which contain phospholipids high in polyunsaturated fatty acids
(PUFAs) are also particularly sensitive.
In meat preparation, mincing destroys the cell membranes and increases the surface exposed
to oxygen therefore increasing the risk of oxidation. A further detrimental factor is the addition
of sodium chloride during preparation, which is common in products such as sausages.
2
Consequences of lipid oxidation on meat quality
•
Off-flavor formation
Lipid oxidation degrades polyunsaturated fatty acids to volatile short-chain compounds such
as aldehydes, ketones, alcohols, esters and acids.
These compounds cause undesirable odors and flavors which strongly reduce the acceptability
of the product by consumers. During cooking and subsequent storage, lipid oxidation in
meat products is enhanced. This phenomenon, referred to as ‘Warmed over Flavor’, is a major
concern for pre-cooked meats.
Cholesterol oxidation
Cholesterol is a component of cell membranes. ‘Cholesterol Oxidation Products’ (COPs)
are detected at trace levels in raw meat while in storage. During cooking and irradiation the
occurrence of COPs is enhanced due to an increase in the generation of free radicals, which
arises due to the oxidation of PUFA’s.
COPs can cause adverse biological effects such as atherosclerosis, cytotoxicity, mutagenesis
and carcinogenesis.
•
Drip loss
At the onset of rigor mortis, pH levels fall, myosin becomes denatured and actomyosin is
formed. This causes a post-mortem shortening of myofibrils and promotes exudative loss
from meat.
Oxidative processes can affect the ability of the membranes to function as a semi-permeable
barrier and may contribute to fluid leakage or drip loss (Jensen, 1998). For example, in fresh
pork meat drip loss tends to increase during refrigerated storage and may cause product
weight losses of 8-12 per cent (Dirinck et al., 1996, Monahan et al., 1994).
•
Muscle pigment oxidation
Color is the main factor affecting meat appearance at the time of purchase. The quality of this
color is dependent on the chemical state of the muscle pigment, myoglobin.
Myoglobin can exist in a ferrous oxygenated form, oxymyoglobin, which produces a cherry-red
color. Alternatively, it can be found in a ferric oxidized metmyoglobin form, which is brownish-
red in color (Faustman and Cassens, 1990). During storage and retail display, oxymyoglobin is
oxidized to metmyoglobin, with the meat turning an undesirable brown color.
3
The antioxidant system
Living organisms have developed specific antioxidant mechanisms which protect against reactive
species. It is only through the presence of antioxidants that living organisms can survive in an
oxygen-rich environment. These mechanisms are described by the general term ‘antioxidant
system’ (Halliwell and Gutteridge, 2007; Surai, 2002).
Antioxidants can be defined as “any substance that delays, prevents or removes oxidative damage
to a target molecule” (Halliwell and Gutteridge, 2007). They are divided into two categories, based
on specific key characteristics:
•
Enzymes:
–
Superoxide Dismutase (SOD)
–
Catalase
–
Glutathione Reductase
–
Glutathione Peroxidase (GPX)
•
Non-enzymatic:
–
Glutathione
–
Uric Acid
–
Vitamin C
–
β-carotene
–
Vitamin E
Based on their physical properties, antioxidants can also be categorized as:
•
Water-soluble antioxidants:
–
Vitamin C
–
Glutathione
–
Uric acid
•
Lipid-soluble antioxidants:
–
Vitamin E
–
β-carotene
Vitamin E: chemistry and metabolism
Vitamin E is a generic term used to describe eight lipid-soluble compounds found in nature.
Four of these compounds are called tocotrienols and the other four tocopherols. These compounds
are isomers and differ from each other by their chemical structure. Tocopherols have higher
efficacy than tocotrienols. In particular α-tocopherol is the most common and, biologically, most
active form.
Vitamin E is supplemented in the diet as the ester of all-rac α-tocopherol. This ester, all-rac
α-tocopheryl acetate, is characterized by greater storage, feed processing and passage stability
through the digestive tract of animals. Pancreatic esterases rapidly release the native α-tocopherol
for absorption from the small intestine (Faustman et al., 1998).
Studies conducted on the role and requirements of vitamin E are typically performed with
commercially available all-rac α-tocopheryl acetate.
4
An extensive body of research has provided detailed information about vitamin E’s exact
metabolic function:
1.
Vitamin E is absorbed by epithelial cells in the small intestine, where it is incorporated
into chylomicrons
2.
It is then transported via the intestinal lymph to the liver
3.
From the liver cells it is secreted by an α-tocopherol transfer protein into general circulation
4.
Finally, it is deposited into the membranes and sub-cellular structures, where it exerts its
protective effects against phospholipids peroxidation
The role of vitamin E in the antioxidant system
An antioxidant system is made of various compounds, located in different cellular, sub-cellular
and extra-cellular spaces and providing different levels of defense. Each antioxidant plays a
specific role in the system and interacts with other compounds in a unique way. It is therefore
important that all these compounds are present in the system; one cannot replace another.
The antioxidant system basically works at three different levels of defense:
•
First level
Responsible for the prevention of free radicals formation by antioxidant enzymes such
as SOD and GPX
•
Second level
Combats the production of free radicals and is made of chain-breaking antioxidants such
as vitamin E, β-carotene, vitamin A, vitamin C and uric acid
•
Third level
Activated for eliminating or repairing the molecules damaged by free radicals. It primarily
consists of enzymes such as lipases, proteases, nucleases and various transferases.
The location of vitamin E in the membrane allows it to function very efficiently in protecting
highly oxidisable polyunsaturated fatty acids from peroxidation by reactive oxygen species
(Liu et al., 1995). The molar concentration of vitamin E in the membranes is lower compared to
phospholipids present. However, it is particularly efficient due to the fact that oxidized vitamin
E can be converted back into the active form. It does this by reacting with other antioxidants
like vitamin C and / or carotenoids.
The chain-breaking antioxidant function of vitamin E is very strong and specific: it stops the
self-perpetrating production of lipid peroxides (Benzie, 1996). However, for optimum efficacy
in preventing lipid oxidation, vitamin E needs to be supplemented in feed at higher levels
than usually given as the vitamin E which is not used for metabolic purposes is going to be
deposited in the cellular membranes. When added to meat post-mortem, the vitamin will not
be physiologically and naturally incorporated in cellular membranes (Liu et al., 1995).
5
Vitamin E and oxidative stability of meat
Several research papers have demonstrated the mode of action and effect of vitamin E in reducing
lipid oxidation and improving meat quality. It has also been demonstrated vitamin E improves
the fluidity of membranes and therefore reduces drip loss. The biggest effect in this area can be
measured in frozen meat, where crystals penetrate the cell membrane and facilitate the leakage
of the cytosol.
•
Poultry
In a recent trial (Barroeta 2007) carried out on broilers, 200mg of vitamin E per kg of feed
was found to reduce the development of thiobarbituric acid reactive substances (TBARS) –
a byproduct of lipid peroxidation – by between 84 and 88 per cent. The production of oxidized
cholesterol compounds in chicken meat was also found to lower by 50 per cent. In addition,
it has also been established that higher levels of vitamin E in feed reduces the concentration
of secondary oxidation products, such as aldehydes and ketones, by around 50 per cent.
•
Swine
The same levels of improvement have been found in the oxidative stability of pig meat
(Buckley et al., 1995; Morrissey et al., 1996; Morrissey et al., 1998). A positive vitamin E
antioxidant effect has been observed when supplemented at 200 mg per kg of feed in pig
rations fortified with 3 per cent soy oil and tallow (Monahan et al., 1992).
A comprehensive review published in 2001 analyzed and summarized 10 studies conducted
between 1991 and 1998 which assessed nutritional impacts on pork quality (Pettigrew and
Esnaola). The review found a consistent improvement of pork meat oxidative stability when
pigs received 100 to 200 mg per kg feed of vitamin E.
•
Cattle
An analysis of 13 studies in cattle and 10 studies in pigs by Sales and Koukolová V. (2011),
assessing the effects of vitamin E supplementation on muscle a-tocopherol levels, lipid
oxidation and meat color found the rate of accumulation was slower in cattle than in pork meat.
Data from swine indicated that tissue saturation in α-tocopherol was reached when feeding
200 to 500 mg per kg of diet. Reinforcing previous studies (Arnold et al., 1993), beef muscle
α-tocopherol concentration could be increased from 1.4 to 3.3 μg/g of meat by feeding at
least 1,300 mg/d of vitamin E for 44 days.
Data also indicated that a muscle α-tocopherol value >3 μg/g of meat was a threshold value
for maximally retard metmyoglobin formation, and related color change, in beef muscle.
•
Meta-analysis studies
More recently, strong confirmation of the positive effect of dietary vitamin E levels on lipid
oxidation has been provided by a meta-analysis (Trefan L. et al., 2011). The authors analyzed
10 published experiments where lipid oxidation was measured and 13 where vitamin E
accumulation was evaluated, in both cases using
M. longissimus dorsi
muscle. The scope
of the analysis was to determine the relationship between dose and duration of vitamin E
supplementation and evolution of oxidative processes in post-slaughter muscle.
6
This meta-analysis established a quantitative relationship between dietary vitamin E and
its effects on pork meat quality. A maximum accumulation in muscle tissue was achieved
at ca. 6.4mg α-tocopherol per gram of tissue. At least 100 mg vitamin E per kg of feed was
required to gain a significant decrease in lipid oxidation and every 1 mg of α-tocopherol per
gram of tissue decreased lipid oxidation by ca. 0.05 TBARS units in
M. longissimus dorsi
.
The meta-analysis also indicated that lipid oxidation gradually increased over three to
four days storage post-slaughter and then stabilized up to 10 days post-slaughter.
•
Improving color stability in pork
The same authors carried out a meta-analysis on the effects of dietary vitamin E and storage
conditions on the color stability of pork meat (Trefan L. et al., 2010). The analysis found a
linear relationship between redness and α-tocopherol concentration. The model revealed that
an increase of 1mg of α-tocopherol in the muscle led to an expected increase of 0.11 in redness
across all storage times. Overall, the meta-analysis suggested that vitamin E supplementation
affected redness of pork, but only when supplementation exceeds 100 mg per kg of feed and
after six days post-slaughter.
•
Reducing drip loss in swine
A meta-analysis of the impact of vitamin E on enhancing pork meat’s water holding capacity
(Apple, 2007) recorded the following results:
Dietary vitamin E supplementation
(mg/kg feed)
Water-holding capacity improvement
(per cent)
100
10.1
200
30.5
Above 400
25.9
The analysis’ author recommended that pigs should be fed a level of 200 mg of vitamin E per
kg of feed for 84 to 130 days before slaughter. Much higher levels (750 to 1.000 mg/kg feed)
could be fed for a minimum of 45 days in order to achieve a minimum threshold concentration
of 2.6mg α-tocopherol per gram of meat tissue (Asghar et al., 1991; Dunshea et al., 2005)
Conclusion
The susceptibility of meat to lipid oxidation is influenced by the α-tocopherol content of the
meat and the PUFA content of the membrane phospholipids. The beneficial effects of vitamin E
on enhancing both poultry and pork meat quality, which stem from its membrane antioxidant
properties in the lipid environment are scientifically proven and commercially tested, validated
and implemented.
This is attributed to the ability of dietary vitamin E, after ingestion and absorption, to deposit and
accumulate in meat. Therefore, vitamin E being the nature’s most effective lipid-soluble, chain
breaking antioxidant, its unique function of protecting cellular membrane integrity cannot be
replaced by other antioxidants or substances possessing antioxidant-like properties.
7
Literature Cited
Apple J.K. (2007) ‘Effects of nutritional modifications on the water-holding capacity of fresh pork:
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, vol 124, (Suppl. 1) pp. 43-58
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nternational Journal of Food Science and Nutrition
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[Hgreen56]

I dont think you want to take vitamin E.
it triggers serotonin and lowers metabolism

 

[Tristan Loscha]

I dont think you want to take vitamin E.
it triggers serotonin and lowers metabolism

I dont know enough about the Serotonin Angle,how does it lower metabolism?Do you mean met is running more efficiently and thus lowering Caloric need or do you see VE as antimetabolic?VE is seen as ergogenic and the main membrane-bound lipid-protector?

 

[Hgreen56]

I dont know enough about the Serotonin Angle,how does it lower metabolism?Do you mean met is running more efficiently and thus lowering Caloric need or do you see VE as antimetabolic?VE is seen as ergogenic and the main membrane-bound lipid-protector?