Vit E 2 x wk. Why?

LucH

Vit E 2 x wk. Why?
Now I rather take twice a week Vit E 400 UI, depending on my status (low-grade inflammation or not).
Why?

We need 20-25 UI per day, according to Chris Masterjohn, in the flower of age (let’s say up to 45 years old).
Half-life of Vit E is rather short (3-4 hours in the blood, to at least 20 hours in tissue) but it could accumulate in liver (quinones). We are going to accumulate if we take 400 UI every day.
Vit K E ALA (α-lipoic acid) and Q10 are some members of the same family.
Tocos are very useful but HD tocos have side-effects: too much of a good thing is bad.

High dose Vit K can interfere with Vit E and vice-versa. Why?
Preambule
I recently read this post:
“Preventing Lipid Peroxidation with Tocotrienols: themselves an unsaturated form of Vitamin E”.
https://bioenergetic.forum/post/66269 (from AlphaZance).
In short, tocotrienols target multiple pathways involved in liver cell damage and lipid accumulation. OK, I agree. But … Shortly said, too much of a good thing is bad. I won’t take only one kind of toco, except in cure, with a specific target, e.g. against virus, inflammation …

Short explanation:

Anything exceeding metabolic needs places a burden on the liver. Derivatives (quinones) unnecessarily saturate elimination pathways (CYP450) and deplete molecules needed elsewhere—particularly for endogenous detoxification (via glutathione S-transferase).
An effective and safe product must contain the full spectrum (totum) or a mixture of at least two natural isomers (e.g. alpha + gamma) to respect cellular efficacy and avoid enzymatic competition. The body prioritizes alpha-tocopherol, yet we also require the other forms. There are eight isomers: alpha, beta, delta, and gamma tocopherols and tocotrienols.
The half-life of vitamin E ranges from 48 to 60 hours. Spacing out doses (every 2 or 3 days) is more than sufficient to maintain a steady state.
The body needs vary from additional 20-25 UI (Chris Masterjohn) to 150 UI (Ray Peat), and more if you follow a diet, losing weight (to neutralize AA cascade).

Excess tocopherols antagonizes Vit K
They are all fat-soluble vitamins and can compete with each other for absorption into the micelle. We could simplify by saying vitamins A and E are antagonists of vitamin K because they interfere with its absorption and metabolism.
Taking a high dose Vit K2 requires transporters that are in limited amount for transport in circulating lipoproteins for subsequent uptake by tissues.
How much is too much is not clearly defined.
The reduction in assimilation appears to be partly related to the phenomenon that Vitamin E and K share similar transporters/metabolizing enzymes. When high dose Vitamin E is given it may block the transporters/enzymes that are needed to integrate Vitamin K into the appropriate tissues. So similar to Aspirin, we should consider supplementing Vitamin K when trying high dose Vitamin E. Otherwise we may risk Vitamin K deficiency which can cause downstream problems.
Moreover excess Vit E, K and Q10 leaves quinones but our liver has a limited capacity to deal with, as already metioned.
I never take Vit A supplement at the same time as the other lipovitamins. Nor 5 000 Vit D with K at the same meal since we need a lot of fat to absorb Vit K (35 gr lipid is optimal: 14 – 25 – 35 g fat are thresholds impacting the degree of absorption. I target minimum 25 g fat).
Edit: Now I limit my intake of Vit K to 1 000 mcg K2 MK4 twice a day, with 1 000 UI Vit D3, both at the same time, so that I don’t saturate the transporter, and so I enhance interaction. Twice a week, I differ the intake to the next meal, because I take 5 000 UI retinyl palmitate. Interaction between liposoluble vitamins.
See additional info on the links beneath.

LucH

*) Sources and references

Kinetic, Bioavailability, and Metabolism Study of RRR-α-Tocopherol in Healthy Adults J Nutr. 2012
Vitamin E may be stored and remain in your body for days, weeks, or even months after you ingest it.
Alpha-tocopherols are preferably stored in the liver and has a double life-time compared to other isomers. The Kinetic, bioavailability, and metabolism study of RRR-α-tocopherol in healthy adults suggests lower intake requirements than previous estimates. The model estimated residence time and half-life of the slowest turning-over compartment of α-tocopherol (adipose tissue) at 499 ± 702 d and 184 ± 48 d, respectively.
https://doi.org/10.3945/jn.112.166462
Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status.
http://www.ncbi.nlm.nih.gov/pubmed/15213041
=> High doses of vitamin E may antagonize vitamin K.
Haemorrhagic toxicity of a large dose of alpha-, beta-, gamma- and delta-tocopherols, ubiquinone, beta-carotene, retinol acetate and L-ascorbic acid in the rat.
http://www.ncbi.nlm.nih.gov/pubmed/7867999
=> These results suggest that the four naturally occurring tocopherols have a tendency to cause haemorrhage in the order of alpha > beta > gamma > delta, and ubiquinone Q-10 and beta-carotene also have relatively strong and weak haemorrhagic effects, respectively, with regard to prothrombin and partial thromboplastin time indices.
Interaction of vitamins E and K: effect of high dietary vitamin E on phylloquinone activity in chicks.
http://www.ncbi.nlm.nih.gov/pubmed/9285253
=> The inhibiting effect of high dietary vitamin E (alpha-tocopherol) on pro-coagulant factors could be prevented by increasing dietary phylloquinone (Vit K1) supplementation. Increased phylloquinone levels in the diet did not significantly influence alpha-tocopherol concentrations in plasma and liver, but coagulopathy caused by high vitamin E intake could be reversed.
Vitamin E decreases extra-hepatic menaquinone-4 concentrations in rats fed menadione (K3) or phylloquinone (K1)
http://www.ncbi.nlm.nih.gov/pubmed/22707266
Vitamin K1 = phylloquinone, K2 = menaquinone, K3 = menadione, and menaquinone-4 (also known as K2 MK4).

LucH

*) Additional info

Vit E: sparing effect and recycling (In French; translator needed)
http://mirzoune-ciboulette.forumactif.org/t30-vitamine-e-plus-qu-une-vitamine#60
"Vitamin C regenerates vitamin E, and vitamin E protects β-carotene—a process aided by polyphenols. With β-carotene supplementation, vitamin C regenerates both vitamin E and β-carotene, and β-carotene appears to protect vitamin E, although the actual mechanism behind this phenomenon remains unexplained."
Savings effect
Vitamin E is not just a vitamin. Vitamin C makes it possible to recycle oxidized vitamin E and thus prolong its lifespan. The same goes with glutathione which is thus saved for other more useful functions (detox). Glutathion is our antioxidant master.
Vitamin E protects against the deleterious effects of polyunsaturated fatty acids when the latter are excess. And this is quickly done!
English corner: How Does Vit E Regulate Redox interactions?
Breaking the ROS chain-reaction from PUFA
https://mirzoune-ciboulette.forumactif.org/t2081-english-corner-how-does-vit-e-regulate-redox-interactions#29973
RP advised 100 UI Vit E (+/ 150 mg) though our requirement increases with age, as our tissue iron stores increase…
Since vitamin E has a half-life of about 48 hours, it could be advisable to take 75 IU - 100 IU orally when there suspicion of Sars-Cov-2. This study also found that alpha-tocopherol (vitamin E) was about 100-fold more potent/effective than Remdesivir against SARS-CoV-2 and other coronaviruses!
https://www.news-medical.net/news/20210715/Water-soluble-vitamin-E-compounds-directly-inhibit-SARS-CoV-2-replication-and-synergize-with-remdesivir.aspx
NB: vitamin E appear to be one of the substances having the ability to inhibit the proliferation / replication as well as the infection once it has already occurred. So do zinc, glycine, naringening, quinine and vitamin D.
Too much of a good thing is bad
There no real danger with high dose vitamin E. But high repeated doses of vitamin E inhibit platelet aggregation. Need to be compensate with K1. Not taken at the same meal (transporters).
Alpha-tocopherol is preferably stocked in the liver. (Kayden and Traber, 1993; Traber et al., 1990).
Every 72 hours would be fine with 400 UI (at least 2 toco). 20-25 UI are needed per day, according to Chris Masterjohn.
Note: As the mechanism by which phylloquinone (K1) is converted to K2 MK-4 is unknown, we cannot readily speculate how vitamin E supplementation influences the concentrations of these forms of vitamin K in extrahepatic tissue. While it is plausible that less MK-4 is produced because vitamin E supplementation reduces phylloquinone as a substrate in the extrahepatic tissue, vitamin E may also decrease MK-4 concentrations independently of phylloquinone.
NB: Vit E and K use the same transporter. So don’t take these supplements at the same time.
More info on Vit E
https://mirzoune-ciboulette.forumactif.org/t30-vitamine-e-plus-qu-une-vitamine#60
Excerpt 1 (translator needed, in French):
Most studies show a beginning of preventive efficiency at doses of 100 IU /d in degenerative diseases. Braking of oxidative stress which is underlying the phenomena of senescence and the appearance of all degenerative pathologies: cardiovascular, cancers, osteoarthritis, osteoporosis, presbyacousis, cataract, macular degeneration, Parkinson and Alzheimer's diseases, etc…
Excerpt 2:
Optimal contribution, without pathology, if under 40 years old: 100 IU per day.
Contribution in case of supplementation in polyunsaturated fatty acids 100 IU per gram of EPA. - Therapeutic contribution: 400 - 500 IU every 5 days.
Mg/ UI conversion: 100 mg = 150 IU.
Personally, it’s 400 UI mixed toco every 3 days (+/ twice a week). 3x if inflammation.
Now Foods – E 400 – with mixed tocopherols. Softgels. + Once a week K1 (mix K1 and K2). Vit K2 MK7 must be encapsulated (oxidation).