all things vitamin E

[NHE]

Vitamin E
http://www.thisisms.com/forum/natural-a ... 18635.html

Vitamin E intake high - is it a problem?
http://www.thisisms.com/forum/natural-a ... 18636.html

Vitamin E and Selenium increase the risk of Prostate cancer
http://www.thisisms.com/forum/natural-a ... 18637.html

[jimmylegs]

Cerebrospinal fluid levels of alpha-tocopherol in patients with multiple sclerosis (1998)
http://www.sciencedirect.com/science/ar ... 409800370X
"The mean CSF vitamin E levels and the CSF/serum vitamin E ratio did not differ significantly between the two study groups. The serum levels of vitamin E and the serum vitamin E/cholesterol ratio were significantly lower in MS patients when compared with controls (P<0.05 and P<0.01, respectively)."

Nonenzymatic antioxidants of blood in multiple sclerosis (1999)
http://www.springerlink.com/content/dflv5gx818uhy8dd/
We investigated the plasma level of lipid peroxides ... (glutathione, α-tocopherol, retinol, plasma sulfhydryl groups, and uric acid) in multiple sclerosis patients with exacerbation or in remission, including a group treated with β-interferon. ... the ratio of plasma α-tocopherol to cholesterol plus triglyceride was decreased (P < 0.001). ... β-Interferon increased plasma α-tocopherol levels (P < 0.001) (:roll:)

Measurement of Low-Molecular Weight Antioxidants, Uric Acid, Tyrosine and Tryptophan in Plaques and White Matter from Patients with Multiple Sclerosis (1992)
http://content.karger.com/ProdukteDB/pr ... tNr=234298
The levels of the antioxidants ascorbic acid, cysteine, reduced glutathione and a-tocopherol, of the free-radical marker uric acid and of the amino acids tyrosine and tryptophan were measured by means of high-pressure liquid chromatography in plaques, adjacent white matter and distant white matter from patients with multiple sclerosis, and in central nervous system tissue from patients without neurological diseases. ... α-tocopherol was lowest in plaques and highest in distant white matter in all cases.

(i know i have posted this next study elsewhere ... wish i could see the full data regarding the values for vitamin e, since we all know my opinion of the value of 'international normal ranges' is so very high :S ):
SELENIUM, VITAMIN E AND COPPER IN MULTIPLE SCLEROSIS (1976)
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
There has been accumulation of the nutritional muscular dystrophy of the cattle in a certain western district of Finland where the prevalence of multiple sclerosis (MS) is also highest. This animal disease is due to lack of selenium (Se) and vitamin E. The Se content of whole blood was low (52.8 ± 11.3 ng/ml) in MS patients from this high-risk area compared to the controls (68.8 ± 11.0). The data for serum failed to confirm this tendency. All Se values appeared to he lower than international values suggested. The values for hoth vitamin E and copper were within the international normal range.

Vitamin E in Humans: Demand and Delivery (1996)
http://www.annualreviews.org/doi/abs/10 ... 196.001541
"How much vitamin E is enough? An established use of supplemental vitamin E in humans is in the prevention and therapy of deficiency symptoms. ... In healthy individuals, a daily intake of about 15-30 mg of α-tocopherol is recommended to obtain “optimal plasma alpha-tocopherol concentrations” (30 μM or greater)."

[jimmylegs]

excellent detailed article on vitamin E

Newly Discovered Benefits of Gamma Tocopherol (2002)
http://www.lef.org/magazine/mag2002/oct ... ma_01.html

subtitles..

Report
"Since taking large doses of alpha tocopherol depletes plasma levels of gamma tocopherol, the health-conscious consumer who takes only alpha tocopherol supplements needs to seriously reconsider this practice. Likewise, most vitamin E supplements provide only alpha tocopherol. New evidence strongly suggests that this is inadequate supplementation."

Anti-inflammatory properties of gamma tocopherol

Protection against prostate and other cancers

Gamma tocopherol's role in cardiovascular disease
"In rats, gamma tocopherol supplementation led to a more potent decrease in platelet clumping and clot formation than supplementation with alpha tocopherol (but it should be remembered that supplementing with gamma tocopherol raises the levels of both gamma and alpha tocopherol). Gamma tocopherol was also a more effective inhibitor of ex-vivo lipid peroxidation, LDL oxidation and superoxide generation. Likewise, gamma tocopherol more effectively enhanced the superoxide dismutase (SOD) expression and activity.[7]
Both alpha and gamma tocopherol increased the generation of nitric oxide, or NO, (NO causes the dilation of blood vessels) by increasing the activity of endothelial nitric oxide synthase. However, only gamma tocopherol supplements led to enhanced protein expression of this crucial enzyme."

Other benefits

Sources of gamma tocopherol

"Please remember that taking large amounts of alpha tocopherol lowers the plasma levels of gamma tocopherol; taking gamma tocopherol, on the other hand, increases the levels of both alpha tocopherol and gamma tocopherol. Taking only alpha tocopherol supplements results in gamma tocopherol depletion.
It will take controlled human studies using gamma tocopherol supplementation to explore its benefits more fully"

References

quotes from one of the referenced articles (pre-dates the flawed SELECT supplementation trial by 8 years)

"A total of 117 of 145 men who developed prostate cancer and 233 matched control subjects had toenail and plasma samples available for assays of selenium, alpha-tocopherol, and gamma-tocopherol. The association between the micronutrient concentrations and the development of prostate cancer was assessed by conditional logistic regression analysis. All statistical tests were two-sided."
...
"For gamma-tocopherol, men in the highest fifth of the distribution had a fivefold reduction in the risk of developing prostate cancer than men in the lowest fifth (P:(trend) =.002)."
...
"Statistically significant protective associations for high levels of selenium and alpha-tocopherol were observed only when gamma-tocopherol concentrations were high."

[jackD]

GOD's gift to neurons -> Tocotrienols

jackD

p.s. Find some FULL-Spectrun ones.

The contents should be listed as shown below.

Tocomin® Full-Spectrum Natural 192 mg
Tocotrienol/Tocopherol Complex

Typical Distribution:

Gamma tocotrienol ........... 38.4-46.08 mg
Alpha tocotrienol..............21.12-26.88 mg
Delta tocotrienol...............10.56-13.44 mg
Beta tocotrienol......................... 2.88 mg
Alpha tocopherol............... 19.2-26.88 mg

Ann N Y Acad Sci. 2004 Dec;1031:127-42.

Tocotrienol: the natural vitamin E to defend the nervous system?

Sen CK, Khanna S, Roy S.
SourceDavis Heart & Lung Research Institute, 473 West 12th Avenue, The Ohio State University Medical Center, Columbus, Ohio 43210, USA.

Abstract
Vitamin E is essential for normal neurological function. It is the major lipid-soluble, chain-breaking antioxidant in the body, protecting the integrity of membranes by inhibiting lipid peroxidation. Mostly on the basis of symptoms of primary vitamin E deficiency, it has been demonstrated that vitamin E has a central role in maintaining neurological structure and function.

Orally supplemented vitamin E reaches the cerebrospinal fluid and brain. Vitamin E is a generic term for all tocopherols and their derivatives having the biological activity of RRR-alpha-tocopherol, the naturally occurring stereoisomer compounds with vitamin E activity.

In nature, eight substances have been found to have vitamin E activity: alpha-, beta-, gamma- and delta-tocopherol; and alpha-, beta-, gamma- and delta-tocotrienol.

Often, the term vitamin E is synonymously used with alpha-tocopherol.

Tocotrienols, formerly known as zeta, , or eta-tocopherols, are similar to tocopherols except that they have an isoprenoid tail with three unsaturation points instead of a saturated phytyl tail. Although tocopherols are predominantly found in corn, soybean, and olive oils, tocotrienols are particularly rich in palm, rice bran, and barley oils.

Tocotrienols possess powerful antioxidant, anticancer, and cholesterol-lowering properties.

Recently, we have observed that alpha-tocotrienol is multi-fold more potent than alpha-tocopherol in protecting HT4 and primary neuronal cells against toxicity induced by glutamate as well as by a number of other toxins.

At nanomolar concentration, tocotrienol, but not tocopherol, completely protected neurons by an antioxidant-independent mechanism. Our current work identifies two major targets of tocotrienol in the neuron: c-Src kinase and 12-lipoxygenase.

Dietary supplementation studies have established that tocotrienol, fed orally, does reach the brain. The current findings point towards tocotrienol as a potent neuroprotective form of natural vitamin E.

PMID:15753140[PubMed - indexed for MEDLINE]

[jimmylegs]

Natural forms of vitamin E: metabolism, antioxidant, and anti-inflammatory activities and their role in disease prevention and therapy (2014)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4120831/
"Highlights
•This is a comprehensive review of various forms of vitamin E.
•γ- and δ-tocopherol and tocotrienols inhibit multiple proinflammatory pathways.
•Long-chain vitamin E metabolites have unique anti-inflammatory effects.
•γ- and δ-tocopherol and tocotrienols are beneficial for disease prevention/treatment.
Abstract
The vitamin E family consists of four tocopherols and four tocotrienols. α-Tocopherol (αT) is the predominant form of vitamin E in tissues and its deficiency leads to ataxia in humans. However, results from many clinical studies do not support a protective role of αT in disease prevention in people with adequate nutrient status. On the other hand, recent mechanistic studies indicate that other forms of vitamin E, such as γ-tocopherol (γT), δ-tocopherol, and γ-tocotrienol, have unique antioxidant and anti-inflammatory properties that are superior to those of αT in prevention and therapy against chronic diseases. These vitamin E forms scavenge reactive nitrogen species, inhibit cyclooxygenase- and 5-lipoxygenase-catalyzed eicosanoids, and suppress proinflammatory signaling such as NF-κB and STAT3/6. Unlike αT, other vitamin E forms are significantly metabolized to carboxychromanols via cytochrome P450-initiated side-chain ω-oxidation. Long-chain carboxychromanols, especially 13′-carboxychromanols, are shown to have stronger anti-inflammatory effects than unmetabolized vitamins and may therefore contribute to the beneficial effects of vitamin E forms in vivo. Consistent with mechanistic findings, animal and human studies show that γT and tocotrienols may be useful against inflammation-associated diseases. This review focuses on non-αT forms of vitamin E with respect to their metabolism, anti-inflammatory effects and mechanisms, and in vivo efficacy in preclinical models as well as human clinical intervention studies."

my pre-dx diet was low in vit E (among other things) and after reading about and implementing the klenner protocol (which was modified in my case, which long predates currently available info on E complex benefits, and which included 2400 IU/d (in divided doses) of a suboptimal alpha tocopherol form) the sensory ataxia / loss of proprioception in my hands resolved within three days.
sample foods http://www.whfoods.com/genpage.php?tnam ... #foodchart
sample supplement http://newrootsherbal.com/product/id/1096

[jimmylegs]

interesting..

Increasing serum levels of vitamin A, D and E are associated with alterations of different inflammation markers in patients with multiple sclerosis (2014)
http://www.jni-journal.com/article/S016 ... 7/abstract

"To explore the relationships between vitamin A, D and E and inflammation in relapsing remitting multiple sclerosis, we assessed their associations with 11 inflammation markers in 9 serial serum samples from 85 patients, before and during interferon-β1a treatment. A negative association was found between vitamin A and pentraxin 3 independent of interferon-β1a use, whereas positive associations between vitamin D and interleukin-1 receptor antagonist and secreted frizzled-related protein 3 were seen before, and between vitamin E and chemokine (C-X-C motif) ligand 16 during interferon-β1a treatment. These findings suggest associations with diverse inflammatory pathways, which may be differentially influenced by interferon-β1a treatment."

also - an older study, previously posted elsewhere at TiMS over the last few yrs:

Alpha-tocopherol and NADPH in the erythrocytes and plasma of multiple sclerosis patients. Effect of interferon-beta-1b treatment (2003).
http://www.ncbi.nlm.nih.gov/pubmed/14634265

"...OBJECTIVES:
To investigate the influence of interferon-beta-1b (INF-beta-1b) therapy on blood antioxidants (alpha-tocopherol and NADPH) in multiple sclerosis (MS).
... erythrocyte alpha-tocopherol level was reduced (p < 0.001) before treatment, but had regained the control level by 6 months of therapy. ... INF-beta-1b seems to exert a sparing effect toward the erythrocyte alpha-tocopherol content. The fall in NADPH in parallel to the rise in plasma triglycerides suggests stimulation of fatty acid synthesis by INF-beta-1b."

[frodo]

We already knew about vitamin D, but it seems vitE could also delay MS progression.

Vitamin E administration erases an enhanced oxidation in multiple sclerosis

http://www.nrcresearchpress.com/doi/abs ... -2018-0246

Abstract

Systemic peroxidation status has been reported as a pathogenic factor for multiple sclerosis (MS). Systemically elevated oxidation levels are associated with serum lipid peroxidation and somatic telomere length (TL) shortening. We investigated whether vitamin E (VE) administration suppresses peroxidation and improves clinical symptoms in 34 MS patients. We analyzed serum lipid peroxidation and degree of TL in circulating leukocytes of MS patients before and after VE treatment. The oxidation level was enhanced and TL was shortened in MS. The MS population treated with VE 400 mg/day for 3 months showed significantly reduced serum lipid oxidation level with maintenance of TL. These findings showed that systemic peroxidation is associated with the development of MS. Antioxidants such as vitamin E can be candidates for supplementary therapeutic agents for MS.

[Scott1]

Hi,

In the past, I've often mentioned that I use a lot of CoQ10. The form I take is in a soft gel capsule with d-alpha tocopherol. That's a form of vitamin E. I find this combination to be very helpful. I am obviously taking a lot of vitamin E as I consume the CoQ10.

Vitamin E is an all embracing term that refers to eight different compounds, including alpha, beta, delta and gamma tocopherol. In addition, vitamin E can also mean alpha, beta, delta and gamma tocotrienol.

Natural forms have a "d" or "RRR" in the prefix. Synthetic forms have "dl" or "all-rac" in the prefix.

It would be interesting to know what they meant by vitamin E.

Regards,

[jimmylegs]

fascinating old article - i'll have to go looking for references to dowd, in the citations provided for the so-called klenner protocol.

MASSIVE DOSAGE OF ALPHA-TOCOPHEROL IN ALLEVIATION OF MULTIPLE SCLEROSIS* (Dowd, 1949)
https://nyaspubs.onlinelibrary.wiley.co ... .tb55308.x

"Seven patients, ages 32-47, who have been afflicted 31-240 months, have been treated, as private patients, for 5--15 months. Our basis for an attempt at treatment with vitamin E lay, first, in three papers by Wechsler,’ Bicknell and Davison in which improvement was noted, both clinically and histologically, in amyotrophic lateral sclerosis. Histologically, the demyelinization and gliosis of multiple sclerosis is similar to the aforementioned syndrome. Secondly, in our geriatric neuropathologies, with similar histopathologic pictures but less extensive involvement, there was some amelioration of symptoms. It was felt that, possibly, some reversal, with attendant increased function, might be effected in nerve tissue which had not yet become fully gliotic. The report is very incomplete, and no definite conclusions may be drawn. It is “thrown out” to the profession to stimulate further study, especially in view of the natural history and apathetic therapy of this disease.
...
Physical examination revealed the usual picture of intention tremors, asymmetrically hyperactive deep tendon reflexes, loss of abdominal reflexes, positive Babinskis, muscular hypotonia or atrophy, and a wide range of sensory abnormalities. The physical examinations were otherwise noncontributory. Incoordination was present in all patients, and vibratory sense was absent in the lower extremities of two patients.
...
Because of the anti-ischemia properties of alpha-tocopherol, it was thought some improvement might be effected by its use. We used and recommend the following method of management:
(1) The patient was given 300 mg (JL: 450 IU) of “Vita E Injectable” (Vitamin Corp. of America, Newark) intramuscularly daily, in three equal 100 mg. doses (first day, one-half the amount was used). This was continued for 4-7 days, dependent upon the size of the patient and the reaction. No iron may be used with E. Hypertensive and hyperthyroid patients should not receive it because of slightly thyrotropic action and mild initial blood pressure elevation in some cases.
(2) Simultaneously, for relaxant effect, the patient received OW of the following antispastics: prostigmine, tolserol, tubocurarine in oil (Abbott), vinobel, or an antihistaminic. Adequate dosage and necessary precautions should be taken, dependent upon the preparation selected.
(3) The patient received high potency vitamin B complex. We used “Provite B-IVC” or “Combex” with C (2) (P.D.) t.i.d., depending on the patient’s tolerance.
(4) The patient received crude liver extract (Armour), 2-4 Units per week I.M. (JL: how about some zinc maybe)
(5) The patient received treatment for any other unrelated pathology by appropriate therapy; for instance, diet and methionine, as a lipotrope, were employed in a fatty infiltrated liver.
(6) After the first week, the patient was placed upon 400-600 mg. of alpha-tocopherol daily in divided doses which were multiples of the 100 mg capsule. The patient was maintained on other supportive therapy (B-Complex, relaxant, and liver extract).
(7) After two weeks, the supportive therapy was reduced to a maintenance level; the alpha-tocopherol was maintained at a high level; and good corrective muscle and nerve coordination re-education was begun. The “twilight zone” (areas where the nerve tissue is neither completely gliotic nor yet functional) degenerating nerve tissue had been “primed” and re-education of the type used in the Veteran Hospital paraplegic and hemiplegic cases was instituted.
(8) The subsequent courses of therapy depended upon the response of the individual patient. In chronic cases, at least 9 months should elapse before any definite trial can be considered fruitless.
(9) After 3 months, the patient was maintained on 300-600 mg. of alpha-tocopherol.
(10) After relaxation was obtained, so that the corrective therapist could maneuver the muscles, the relaxant was decreased or discontinued. Here again, dosage was an individual problem.

Results
The results were quite revealing. Two cases reverted to virtual normalcy (a few residual paresthesias were left) after 5 and 9 days, respectively, of therapy. These were acute types, which were seen a few days after onset. Each had had several previous bouts which had lasted for 2-2.5 months. The disease had been first noted 2 years before in one and 2.5 years in the other. The remaining 5 cases were chronics. After four weeks of tocopherols, there was less muscle weakness, less atrophy, and decreased paresthe sias and hyperesthesias, deafness disappeared, and better coordination in locomotion was present. After 2-14 months of corrective therapy, along with maintenance tocopherols, ataxia, spasticity, and muscular strength have been moderately improved in 3 patients. Two severe cases have been unaffected as yet.
...
alpha-tocopherol appears to be a useful tool, but not a panacea, which needs further study before its role can be accurately appraised. From a study of the treatment just described, we feel that massive doses of alpha-tocopherol, when used in conjunction with good corrective therapy, offer a worthwhile approach to the management of multiple sclerosis."


when the klenner protocol did me so much good in 2006, i was fixated on the vitamin b aspect. it really did take me quite a while to realize the extent to which the vit e had likely played a role in my own positive experiences with this multi-megadose therapy.

in hindsight i finally realized my diet had been atrocious for vit e leading up to my dx, and then when i first read this info (ages ago now), it made a LOT of sense: https://neuromuscular.wustl.edu/nother/vitamin.htm#e

it worked for me, even using a single synthetic form that i wouldn't use now. improved supplemental forms still a challenge. i can't get buy in from my friend's oncologist re 400iu per day even of E8 complex. green light from food sources only, so it's been all about the various oils.

also fascinating today, to see ophthalmoplegia (@vender, i'm looking at you - with my non-double vision ;) ) noted as a consequence of vit E deficit. when i had my skirmish with INO earlier this year, it was all laid at the feet of MS. nobody said a peep about links to vitamin E.

[NHE]

...and vibratory sense was absent in the lower extremities of two patients.

That sounds like subacute combined degeneration due to B12 deficiency.

[jimmylegs]

indeed.

back in 2006/7 i personally spent a lot of time trying to jam every symptom and piece of evidence into the b12 box.
however, when the multi vit/min klenner protocol helped me, i had already spent months unsuccessfully trying (with b12 alone) to correct previously b12-reversible issues.
no dice.

Vitamin B12 (Cobalamin) deficiency
https://neuromuscular.wustl.edu/nother/vitamin.htm#B12

CNS
Spinal cord: Earliest locus of involvement
Major cause of sensory & motor disability


Vitamin E deficiency
https://neuromuscular.wustl.edu/nother/vitamin.htm#e

CNS
[oct 2020 update - this one bit i skipped over when i posted this excerpt has since become more relevant...:
Ophthalmoplegia]
Spinal
Posterior column sensory loss...

i have not looked into every detail in-depth; at the time, the list of vit e symptoms - in addition to my own back story - made much more sense than b12 alone.

[jimmylegs]

Alpha-tocopherol ameliorates experimental autoimmune encephalomyelitis through the regulation of Th1 cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923477/
"... AT reduced the inflammation and the demyelination reaction in the spinal cord. Treatment with AT significantly decreased the proliferation of splenocytes. AT also inhibited the production of IFN-γ (Th1 cytokine) ... AT ameliorated EAE, through suppressing the proliferation of T cells and the Th1 response. AT may be used as a potential treatment for MS."

[jimmylegs]

revisiting INO and vit E

Acquired Binocular Horizontal Diplopia (1999)
https://www.mayoclinicproceedings.org/a ... 5/fulltext
"... INO, the One-and-a-Half Syndrome, and Vitamin E Deficiency.—Clinically, INO is characterized by adduction weakness on the side of a lesion of the medial longitudinal fasciculus (MLF) and monocular nystagmus of the opposite abducting eye. Convergence is usually preserved unless the responsible lesion is high in the midbrain. Patients with INO often have no symptoms but may complain of horizontal or vertical diplopia (the latter due to associated vertical eye misalignment [skew deviation]). Rarely, XT may occur with unilateral INO (wall-eyed monocular INO or WEMINO syndrome) or with bilateral INO (walleyed bilateral INO or WEBINO syndrome); in the latter, both eyes are deviated laterally.110, 111, 112, 113, 114, 115 Causes of INO include multiple sclerosis, brain-stem infarction or hemorrhage, infections, paraneoplastic disease, and other degenerative, nutritional, and metabolic processes.
...
Vitamin E deficiency may be associated with an ex-traocular motility impairment that superficially resembles the WEBINO syndrome. As in the WEBINO syndrome, the patient demonstrates XT associated with adduction limitation and dissociated horizontal nystagmus on lateral gaze. In vitamin E deficiency, however, saccadic movements are slower in the abducting eye rather than in the adducting eye, and the dissociated nystagmus has greater amplitude in the adducting eye.116 This motility impairment is especially noted with abetalipoproteinemia associated with other findings, including ataxia, weakness, posterior column dysfunction, and pigmentary retinopathy."

i will need to spend more time to get myself up to speed on all this material ...

[jimmylegs]

gonna take a closer look at this one, too

Gamma-Tocopherol – An Underestimated Vitamin? (2004)
https://www.researchgate.net/profile/Ib ... itamin.pdf

i am interested in this bit
" Because recent studies suggest that populations need to increase their intake of vitamin E significantly, from the recommended daily intake 10- to 20-fold [27], ..."

and note that 27, while it may have been recent in 2004...

Grusak MA: Genomics-assisted plant improvement to benefit human nutrition and health. Trends Plant Sci 1999;4:164–166.
https://www-sciencedirect-com.proxy.lib ... 8599014004

"...The adult recommended daily allowance for vitamin E is 8–10 mg α-TE (Ref. 6); this level is thought to be adequate to prevent biological deficiency. However, a growing body of clinical and epidemiological evidence suggests that higher intakes of vitamin E (∼100–250 mg α-TE daily) decreases the risk of cardiovascular disease and cancer, strengthens immune function, and prevents or slows various age-related degenerative diseases7..."

and now for 7... this one was posted some time back:
M.G. Traber, H. Sies. Vitamin E in humans: demand and delivery. Annu. Rev. Nutr., 16 (1996), pp. 321-347
https://www.annualreviews.org/doi/abs/1 ... 196.001541

"...Also discussed is the use of supplemental vitamin E in chronic diseases such as ischemic heart disease, atherosclerosis, diabetes, cataracts, Parkinson's disease, Alzheimer's disease, and impared immune function, as well as in subjects receiving total parenterol nutrition. In healthy individuals, a daily intake of about 15-30 mg of alpha-tocopherol is recommended to obtain "optimal plasma alpha-tocopherol concentrations" (30 microM or greater)..."

so 400 Iu d-alpha tocopherol should about do it, to the tune of about 27 mg at least... (can't get full text on that one, though). i wonder, how much is needed daily to achieve optimal status in less than healthy individuals?

and as for who's been citing grusak, here are a couple of recent ones:

Vitamin E (α- and γ-Tocopherol) Levels in the Community: Distribution, Clinical and Biochemical Correlates, and Association with Dietary Patterns (2018)
https://www.mdpi.com/2072-6643/10/1/3/htm

Gamma tocopherol, its dimmers, and quinones: Past and future trends (2020)
https://pubmed.ncbi.nlm.nih.gov/31957471/

lol spellcheck doesn't know about dimers i guess..

comparing optimal intake per traber et al to health canada's related info:

https://www.canada.ca/en/health-canada/ ... -2005.html

adult rdi 12 to 15 mg, upper limit 1000mg that's right ONE THOUSAND... or 15000 IU. guess i won't worry too much about Hypervitaminosis E
https://neuromuscular.wustl.edu/nother/vitamin.htm#vitE
just yet...!

[jimmylegs]

this 2012 article confused me for a while...!

Vitamin E in ataxia and neurodegenerative diseases: A review (2012)
https://www.scirp.org/pdf/wjns20120400006_46258016.pdf

":2. PHYSIOLOGY
Vitamin E is an essential fat-soluble Vitamin. Recently, the National Academy of Sciences defined Vitamin E as the 2R stereoisomers of alpha-tocopherol. However, past classifications of Vitamin E included a group of eight compounds—alpha-, beta-, gamma- and delta-tocopherols and tocotrienols. The naturally occurring d-alpha-tocopherol has the highest biological activity [1].
...
3.2
...Symptoms of neurological dysfunction develop within 18 - 24 months in children with Vitamin E deficiency but in adults, symptoms may develop after approximately 10 - 20 years of malabsorption [10]; indicating the length of time required for depletion of Vitamin E stores and for accumulation of clinically significant neuronal damage.
...
4.3. Natural-Source vs Synthetic Vitamin E
Vitamin E is the exception to the paradigm that natural and synthetic Vitamins are equivalent. Natural-source Vitamin E (RRR-alpha-tocopherol or d-alpha-tocopherol) is derived from vegetable oils and is a single isomer. Synthetic Vitamin E (all-rac-alpha-tocopherol or dl-alphatocopherol) is a mixture of eight isomers, only one of which is d-alpha-tocopherol. The 2000 National Academy of Sciences report recognizes four of the eight isomers (2R isomers) to have Vitamin E activity and the other four isomers to have none. Physiological differences between natural-source and synthetic Vitamin E relate to preferential retention of dalpha-tocopherol in blood and tissues compared to other tocopherols."

[1] National Academy of Sciences (2000) Dietary reference
intakes for Vitamin C, Vitamin E, selenium and carotenoids. National Academy Press, Washington DC.

contrast

Vitamin E (α- and γ-Tocopherol) Levels in the Community: Distribution, Clinical and Biochemical Correlates, and Association with Dietary Patterns (2017)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793231/

...Vitamin E encompasses 4 tocopherols (α-, β-, γ-, and δ-tocopherol) and 4 tocotrienols (α-, β-, γ-, and δ-tocotrienol), with α-tocopherol representing over 90% of total tocopherol [1,2].
...

1. Sauberlich H.E. Laboratory Tests for the Assessment of Nutritional Status. 2nd ed. CRC Press; Boca Raton, FL, USA: 1999. Vitamin E (Tocopherols) pp. 249–266.
2. Jiang Q. Natural forms of vitamin E: Metabolism, antioxidant, and anti-inflammatory activities and their role in disease prevention and therapy. Free Radic. Biol. Med. 2014;72:76–90. doi: 10.1016/j.freeradbiomed.2014.

Natural forms of vitamin E: metabolism, antioxidant and anti-inflammatory activities and the role in disease prevention and therapy (2014)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4120831/

"The Vitamin E family consists of four tocopherols and four tocotrienols. α-Tocopherol (αT) is the predominant form of vitamin E in tissues and its deficiency leads to ataxia in humans. However, results from many clinical studies do not support protective roles of αT in disease prevention in people with adequate nutrient status. On the other hand, recent mechanistic studies indicate that other forms of vitamin E such as γ-tocopherol (γT), δ-tocopherol (δT) and γ-tocotrienol (γTE) have unique antioxidant and anti-inflammatory properties that are superior to αT in prevention and therapy against chronic diseases.
...
Here we discuss recent development in the field of non-αT forms of vitamin E with respect to their metabolism, antioxidant and anti-inflammatory effects.
...
αT is predominantly found in peanuts, almonds and sunflower seeds, while γT is the major vitamin E in walnuts, pecans, pistachios and sesame seeds [6, 7]. As a result, αT and γT are found in many food oils like corn, soybean and peanut oil (Table 1) [6, 7]. Due to the widespread use of corn and soybean oil, γT represents ~60–70 % vitamin E consumed in the typical US diet, while αT accounts for 20–25% [6]. "

these 2014 and 2017 sources seem much more in line with the impressions i've been operating under for the last decade plus...

as for dietary sources, i would have to work hard to find any corn oil or soybean oil in my own diet. i can't remember where i learned that corn oil was the single oil that contained all 8 tocopherols and tocotrienols, but i've given up trying to find organic corn oil long since. maybe it's time to try again...

will revisit that 2014 article later. a bit much to take in today but at least for now, my earlier surprise at reading the 2012 bit about natural vs synthetic vit E is somewhat allayed...