Balancing Vitamins A And E

Amazoniac

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It's surprising how little discussion there is on this topic. The influence must occur both ways. I don't have it clear yet but hopefully this thread encourages investigation on their interaction and balance.

- https://www.westonaprice.org/health...a-on-trial-does-vitamin-a-cause-osteoporosis/

"Several studies, when taken together, suggest that vitamin E can interfere with the functioning of, or increase the need for, vitamin A. In Nutrition and Physical Degeneration, Weston Price described the importance of vitamin A for the development of eye tissue and cited experiments carried out by Fred Hale, wherein vitamin A-deficient pigs gave birth to offspring with a variety of eye defects, including blindness and in some cases the absence of eyeballs.43 In a more recent study,44 researchers injected the environmental pollutant TCDD, the most potent dioxin, vitamin E as a-tocopherol succinate, and vitamin A as retinol acetate, into eggs containing chicken embryos, and then let the chicks hatch. Vitamin A and vitamin E both protected against TCDD-induced birth defects, but vitamin E caused birth defects of its own – mostly eye abnormalities. One chick, like some of Fred Hale’s vitamin A-deficient pigs, was even born with no eyes.

TCDD, which acts as a hormone and both mimics vitamin A and opposes vitamin A in various ways,45 helped reduce the vitamin E-induced birth defects, but the researchers did not test whether or not vitamin A protected against these birth defects. In humans, vitamin A helps improve the eye disease retinitis pigmentosis, while vitamin E accelerates it.46 If high doses of vitamin E can induce the same eye defects as induced by deficient doses of vitamin A, and if vitamin E accelerates the same eye diseases as are helped by vitamin A, then vitamin E’s toxic effects on the eye may result from a depletion of vitamin A. In fact, excessive doses of the a-tocopherol form of vitamin E not only interfere with the functioning of vitamin A, but actually interfere with the functioning of vitamin E itself, by inhibiting the action of the other important parts of the vitamin E complex.47"

[47] Dommisse, John, “B12: Difficulties and Obstacles in Diagnosing and Treating B12 Deficiency,” Wise Traditions 2005, November 12, 2005.​

- Effects and Interactions of Dietary Levels of Vitamins A and E and Cholecalciferol in Broiler Chickens

"Studies have demonstrated that the feeding of high dietary levels of vitamin A leads to decreased tissue and plasma tocopherol concentrations in chicks (Pudelkiewiczet al., 1964; Combs and Scott, 1974; Combs, 1976; Sklan and Donoghue, 1982; Frigg and Broz, 1984; Abawi and Sullivan, 1989). Conversely, high dietary tocopherol alleviated hypervitaminosis A in chicks (McCuaig and Motzok, 1970; Sklan and Donoghue, 1982)."

"March et al. (1973) reported that with calcium- or vitamin D-deficient diets, bone calcification was depressed when chicks were given excess vitamin E. Similarly, Murphy et al. (1981) observed reduced bone ash and plasma calcium and phosphorus when chicks were given large doses of vitamin E. A significant three-way interaction among vitamins A, D3, and E was noted for plasma vitamin E concentrations in broiler chickens (Abawi and Sullivan, 1989)."

"Although it was not a major objective of these studies to look at the dietary interactions of vitamin A and vitamin E it was clear from the blood levels in Experiment 4 that this relationship does exist. Feeding excess vitamin A decreases the blood and liver levels of vitamin E and feeding excess vitamin E decreases the blood and liver levels of vitamin A. The mechanism of this relationship needs further study."​

- https://raypeatforum.com/community/...erves-of-the-liver-may-be-much-reduced.16124/

Time to search for excess vitamin E and signs of vitamin A deficiency..

All life matters.
 
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Mossy

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A good topic, I'd say. Thanks.
 

Pointless

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Well Ray has said that vitamin E can prevent most of the symptoms of retinol toxicity. Maybe there is no such thing as a "balance" of these nutrients, like an optimal ratio. There is merely a sufficiency, and our demand for vit. A or E increases when taking one or the other. To say more than that, we would need to define optimal functioning of retinol and tocopherols but that seems to depend on pufa load and other factors.
 
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Amazoniac

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Interrelationships between Vitamin E and Other Vitamins and the Ubiquinones

"Moore (1939) first noticed that the vitamin A reserves of tocopherol-deficient rats were invariably lower (by two- to ten-fold) than those of controls given vitamin E, and Davies and Moore (1941) showed that at least part of the effect was due to a protective action on already stored vitamin A. Starting with rats with liver reserves of about 20,000 I.U. of vitamin A, they found that 7 weeks on a diet deficient in both vitamins was sufficient to reduce the reserves almost to zero, whereas rats given vitamin E still contained about 5000 I.U. of vitamin A. Other workers have had similar results, and Dam et al. (1952) found a similar effect in the chick. Most of these later studies, however, have involved not only storage, but problems of absorption and utilization and have generally revealed that the vitamin A-vitamin E relationship is more complicated than would at first appear."

"Popper and Volk (1944) reported that fluorescent microscopic examination of rat intestine showed no increase in absorption of vitamin A after tocopherol administration. Lemley et al. (1947) found that solubilized tocopherols given to rats parenterally had the same effect in supplementing vitamin A activity as when they were given orally, and they suggested that the action of tocopherol could not be limited to the gut. They showed, furthermore, that the timing of the related doses was important. Liver storage of vitamin A was not influenced by tocopherol when measured over 3 days, but only when the experiment was carried out for considerably longer periods. The results of Edwin et al. (1962) also show that the accumulation of vitamin A in several tissues of the rat is markedly dependent on the experimental conditions. They found that, if a single oral dose of vitamin A was given to rats deficient in vitamins A and E, less was taken up than in rats whose diet contained adequate vitamin E. If the vitamin E was given together with the vitamin A, however, very little more (and sometimes less) was absorbed than if the vitamin E was not present."

"Comparatively little is known about the reverse problem, the effect of vitamin A supplementation on vitamin E levels and requirements--perhaps because vitamin E analyses are more difficult to carry out than vitamin A analyses. Although there have been several studies of the marked nutritional antagonism between vitamin E and various fish liver oils, this antagonism is generally considered to be mainly due to the unsaturated fatty acid content of these oils. The results of Diplock et al. (1961) and Edwin et al. (1962), who analyzed several tissues from rats fed diets containing different levels of vitamins A and E, indicate that, as expected, tocopherol levels are depressed when increased vitamin A is given. Dicks et al. (1959) obtained similar results in cattle. Edwin et al. (1962) have commented on the exceptionally high tocopherol levels that are found in the livers of rats in the final stages of vitamin A deficiency."

"Chevrel and Cormier (1948) reported that, rather surprisingly, external signs of vitamin A deficiency in the rabbit appeared only when the animals were also deficient in vitamin E. Butturini (1943) found a remarkable synergism between the two vitamins in creatinuria. In normal rats, 1-10 mg of a-tocopherol every other day for 2 weeks reduced creatinuria to zero; but, if doses of 12,000 I.U. of vitamin A mere given at the same time, as little as 0.1 mg was effective. In vitamin A deficient rats, although either carotene or a-tocopherol reduced creatinuria somewhat, simultaneous dosage with vitamins A and E was necessary to reduce it to zero. In severe vitamin E deficiency, neither vitamin alone was efficient in reducing creatinuria. Edwin et al. (1962) commented that rats deficient in vitamin A and E tended to survive longer than rats deficient only in vitamin A."

"Moore (1940) first reported that vitamin E had less effect on the storage of vitamin A derived from carotene than on the storage of the preformed vitamin. Guggenheim (1944) found that the utilization of plant carotenes depended on the tocopherol content of the tissue and showed that in the rat, fecal elimination (and hence the protection) of carotene was increased in the presence of tocopherol. Harris et al. (1944) gave small marginal doses (approximately 1 mcg) of b-carotene to rats and found that daily doses of 0.5 mg of mixed tocophcrols increased the growth response: larger quantities of tocopherol, however, reversed the effect."

"[..]although small amounts of tocopherol might protect carotene, larger amounts might inhibit a step in the conversion of carotene to vitamin A."

"Holmes and Pigott (1941) reported that the muscular dystrophy of weanling rats on a vitamin E-deficient diet could be relieved by 4-14 I.U. of thiamine per rat. Hickman et al. (1944) suggested that, a deficiency of B vitamins altered the rat’s requirements of vitamin E, and d’Agostino (1952) found that both the blood level and the excretion of thiamine in human subjects was lowered after dosing with 150-600 mg of a-tocopherol."

"Hove and Hardin (1950, 1951) found that vitamin B12 synergized the effect of vitamin E in preventing liver damage in rats due to carbon tetrachloride poisoning, perhaps owing to an indirect action on protein balance. They demonstrated that considerably more vitamin E was necessary to prevent creatinuria if the rats were deficient in vitamin B12 as well. Giacolone (1956) observed a marked reduction within 15 days in the vitamin B12 content of the livers of rats fed a necrogenic diet. Dinning et al. (1954) have studied the interrelationship of vitamin E and pyridoxine in several species. Dinning (1953) found that vitamin E supplements hastened the appearance of pyridoxine deficiency symptoms in rats; but, according to Young (1957), vitamin E prevents the reduction in liver xanthine oxidase activity in pyridoxine-deficient animals."

"Crider et al. (1960) found that the livers of vitamin K-supplemented rats contained increased quantities of a nontocopherol reducing substance, as compared to deficient controls: this substance appears to be ubichromenol(45), and the finding is in general agreement with those of Edwin et al. (1961)."
 

Jon

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@Amazoniac This is just one more reason supplements are sounding more and more risky to me and that a diet which either represents all the micro nutrients or negates the need for some of them is the pinnacle we should all be aiming for. Good find, thanks for keeping us in the know!
 

InChristAlone

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Forgot you posted about this, which is what I was basically saying in the genereux thread that maybe people with supposed VA overload are missing a cofactor. Vitamin E!!
 
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lollipop

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@Amazoniac This is just one more reason supplements are sounding more and more risky to me and that a diet which either represents all the micro nutrients or negates the need for some of them is the pinnacle we should all be aiming for. Good find, thanks for keeping us in the know!
+1 I have also started to come to the same conclusion.
 

Jon

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+1 I have also started to come to the same conclusion.

Im thinking this is why Peat makes sure to throw in that supplementing usually clears up deficiencies "quickly" hoping that people will read between the lines that you should really only be using a supplement for a deficiency and that you don't have to use a supplement very long.
 
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Amazoniac

Amazoniac

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Dietary vitamins A and E influence retinyl ester composition and content of the retinal pigment epithelium

"Experiments were conducted to determine the influence of dietary levels of vitamin levels A and α-tocopherol on the amounts and composition of retinyl esters in the retinal pigment epithelium of light-adapted albino rats. Groups of rats were fed diets containing α-tocopherol and either no retinyl palmitate, adequate retinyl palmitate, or excessive retinyl palmitate. Other groups of rats received diets lacking α-tocopherol and containing the same three levels of retinyl palmitate. Retinoic acid was added to diets lacking retinyl palmitate. After 27 weeks, the animals were light-adapted to achieve essentially total visual pigment bleaches, and the neural retinas and retinal epithelium-eyecups were then dissected from each eye for vitamin A ester determinations. Almost all of the retinyl were found in the retinal pigment epithelium-eyecup portions of the eyes, mainly as retinyl palmitate and retinyl stearate. Maintaining rats on a vitamin A-deficient, retinoic acid-containing diet led to a significant reductions in retinal pigment epithelial retinyl ester levels in rats fed both the vitamin E-supplemented and vitamin E-deficient diets; contrary to expectations, the effect of dietary vitamin A deficiency was more pronounced in the vitamin E-supplemented rats. Vitamin A deficiency in retonic acid-maintained animals also led to significant reductions in retinyl palmitate-to-stearate ester ratios in the retinal pigment epithelia of both vitamin E-supplemented and vitamin E-deficient rats. Excessive dietary intake of vitamin A had little, if any, effect on retinal pigment epithelial retinyl ester content or composition. Vitamin E deficiency resulted in significant increases in retinal pigment epithelial retinyl palmitate content and in palmitate-to-stearate ester ratios in rats fed all three levels of vitamin A, but had little effect on retinal pigment epithelial retinyl stearate content. In other tissues, vitamin E deficiency has been shown to lower vitamin A levels, and its widely accepted that this effect is due to autoxidative destruction of vitamin A. The increase in retinal pigment epithelial vitamin A ester levels in response to vitamin E deficiency indicates that vitamin E does not regulate vitamin A levels in this tissue primarily by acting as antioxidant, but rather may act as in inhibitor of vitamin A uptake and/or storage. The effect of vitamin E on pigment epithelial vitamin A levels may be mediated by the vitamin E-induced change in retinyl palmitate-to-stearate ratios."

I had to invoke a Travo highlight for this.

upload_2018-7-30_13-53-0.png

"Interactions between vitamins E and A in vivo have been recognized for quite some time [11,12]. Both plasma and tissue levels of vitamin A are depressed as a result of vitamin E deficiency [13-15]. This phenomenon may indicate that vitamin E protects vitamin A from autoxidative destruction in vivo [12,16,17], although other explanations have been proposed [18,19]. Both vitamins E and A have been reported to influence the accumulation of a stable autofluorescent pigment, lipofuscin, in the rat retinal pigment epithelium [15,17,20-23]. Lipofuscin accumulation is accelerated by vitamin E deficiency [14,15,17,20-23], and suppressed by vitamin A deficiency [15,23]. These observations suggest that, in the retinal pigment epithelium, vitamin A may be converted into pigment fluorophores, and that such a conversion may be at least partially blocked by vitamin E."

"[..]in the neural retina-retinal pigment epithelial complex, vitamin E interacts with vitamin A compounds in a more complex manner than simply as an antioxidant, in contrast to what would be predicted on the basis of previous studies [11,13-15]. The data are consistent with the possibility that vitamins E and A compete for some common binding sites in the neural retina-retinal pigment epithelium, so that vitamin E may displace some vitamin A from these tissues. Further support for this hypothesis comes from the observation that vitamin A deficiency results in an elevation in neural retinal a-tocopherol content (Table III), suggesting that reduction in retinal vitamin A content may liberate a-tocopherol binding sites. Likewise, vitamin E deficiency significantly retarded the depletion of retinol from the neural retinas of vitamin A-deficient animals (Table III), which is again consistent with the possibility that both vitamins E and A may share binding sites in the neural retina-retinal pigment epithelium. Fong and colleagues [32] have reported that vitamins E and A compete for binding to interphotoreceptor matrix retinol-binding protein, suggesting that this protein may be one site from which vitamin E can displace vitamin A from the eye."

upload_2018-7-30_13-53-7.png

"Another potential explanation for the elevation of retinal pigment epithelial retinyl ester content in vitamin E-deficient rats arises from the possibility that vitamin A esters may be sequestered in retinal pigment epithelial lipofuscin granules. Vitamin E deficiency substantially increases retinal pigment epithelial lipofuscin content [14,15,20-22], whereas retinol deficiency suppresses retinal pigment epithelial lipofuscin deposition significantly [15,23]. Therefore, a strong correlation exists between retinal pigment epithelial lipofuscin content and vitamin A ester levels. A further suggestion that vitamin A esters may be associated with lipofuscin granules in the retinal pigment epithelium is provided by the finding that the retinyl palmitate-to-stearate ester ratios are correlated with lipofuscin content in this tissue. Vitamin A deficiency, which leads to a reduction in retinal pigment epithelial lipofuscin content, also results in a decrease in the palmitate-to-stearate ester ratio (Table V). Vitamin E deficiency, on the other hand, significantly elevates both retinal pigment epithelial lipofuscin content and the ratio of retinyl palmitate to retinyl stearate in the retinal pigment epithelium (Table V [above]). Aging, which is accompanied by an increase in retinal pigment epithelial lipofuscin content [25], also elevates the retinyl palmitate-to-stearate ester ratio in the retinal pigment epithelium [25]. The latter finding provides additional support for the hypothesis that vitamin A esters may be associated with lipofuscin granules. More direct evidence for such an association has been obtained by Feeney-Burns and Eldred [33], who have extracted retinyl esters from partially purified lipofuscin granules isolated from the human retinal pigment epithelium. The observation that the retinyl palmitate-to-stearate ester ratio is higher in retinal pigment epithelia with high lipofuscin contents suggests that the palmitate ester may be preferentially sequestered in lipofuscin granules. This may have implications for the mobilization of vitamin A from retinal pigment epithelial pools for visual pigment regeneration during dark adaptation, particularly if the palmitate and stearate esters of retinol are metabolized differently, or if lipofuscin-associated pools of vitamin A differ in their accessibility from the remainder of vitamin A stores."


The main purpose here is to stress that there has to be a balance between them and that the influence indeed occurs both ways.
 
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Jon

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Dietary vitamins A and E influence retinyl ester composition and content of the retinal pigment epithelium

"Experiments were conducted to determine the influence of dietary levels of vitamin levels A and α-tocopherol on the amounts and composition of retinyl esters in the retinal pigment epithelium of light-adapted albino rats. Groups of rats were fed diets containing α-tocopherol and either no retinyl palmitate, adequate retinyl palmitate, or excessive retinyl palmitate. Other groups of rats received diets lacking α-tocopherol and containing the same three levels of retinyl palmitate. Retinoic acid was added to diets lacking retinyl palmitate. After 27 weeks, the animals were light-adapted to achieve essentially total visual pigment bleaches, and the neural retinas and retinal epithelium-eyecups were then dissected from each eye for vitamin A ester determinations. Almost all of the retinyl were found in the retinal pigment epithelium-eyecup portions of the eyes, mainly as retinyl palmitate and retinyl stearate. Maintaining rats on a vitamin A-deficient, retinoic acid-containing diet led to a significant reductions in retinal pigment epithelial retinyl ester levels in rats fed both the vitamin E-supplemented and vitamin E-deficient diets; contrary to expectations, the effect of dietary vitamin A deficiency was more pronounced in the vitamin E-supplemented rats. Vitamin A deficiency in retonic acid-maintained animals also led to significant reductions in retinyl palmitate-to-stearate ester ratios in the retinal pigment epithelia of both vitamin E-supplemented and vitamin E-deficient rats. Excessive dietary intake of vitamin A had little, if any, effect on retinal pigment epithelial retinyl ester content or composition. Vitamin E deficiency resulted in significant increases in retinal pigment epithelial retinyl palmitate content and in palmitate-to-stearate ester ratios in rats fed all three levels of vitamin A, but had little effect on retinal pigment epithelial retinyl stearate content. In other tissues, vitamin E deficiency has been shown to lower vitamin A levels, and its widely accepted that this effect is due to autoxidative destruction of vitamin A. The increase in retinal pigment epithelial vitamin A ester levels in response to vitamin E deficiency indicates that vitamin E does not regulate vitamin A levels in this tissue primarily by acting as antioxidant, but rather may act as in inhibitor of vitamin A uptake and/or storage. The effect of vitamin E on pigment epithelial vitamin A levels may be mediated by the vitamin E-induced change in retinyl palmitate-to-stearate ratios."

I had to invoke a Travo highlight for this.


"Interactions between vitamins E and A in vivo have been recognized for quite some time [11,12]. Both plasma and tissue levels of vitamin A are depressed as a result of vitamin E deficiency [13-15]. This phenomenon may indicate that vitamin E protects vitamin A from autoxidative destruction in vivo [12,16,17], although other explanations have been proposed [18,19]. Both vitamins E and A have been reported to influence the accumulation of a stable autofluorescent pigment, lipofuscin, in the rat retinal pigment epithelium [15,17,20-23]. Lipofuscin accumulation is accelerated by vitamin E deficiency [14,15,17,20-23], and suppressed by vitamin A deficiency [15,23]. These observations suggest that, in the retinal pigment epithelium, vitamin A may be converted into pigment fluorophores, and that such a conversion may be at least partially blocked by vitamin E."

"[..]in the neural retina-retinal pigment epithelial complex, vitamin E interacts with vitamin A compounds in a more complex manner than simply as an antioxidant, in contrast to what would be predicted on the basis of previous studies [11,13-15]. The data are consistent with the possibility that vitamins E and A compete for some common binding sites in the neural retina-retinal pigment epithelium, so that vitamin E may displace some vitamin A from these tissues. Further support for this hypothesis comes from the observation that vitamin A deficiency results in an elevation in neural retinal a-tocopherol content (Table III), suggesting that reduction in retinal vitamin A content may liberate a-tocopherol binding sites. Likewise, vitamin E deficiency significantly retarded the depletion of retinol from the neural retinas of vitamin A-deficient animals (Table III), which is again consistent with the possibility that both vitamins E and A may share binding sites in the neural retina-retinal pigment epithelium. Fong and colleagues [32] have reported that vitamins E and A compete for binding to interphotoreceptor matrix retinol-binding protein, suggesting that this protein may be one site from which vitamin E can displace vitamin A from the eye."


"Another potential explanation for the elevation of retinal pigment epithelial retinyl ester content in vitamin E-deficient rats arises from the possibility that vitamin A esters may be sequestered in retinal pigment epithelial lipofuscin granules. Vitamin E deficiency substantially increases retinal pigment epithelial lipofuscin content [14,15,20-22], whereas retinol deficiency suppresses retinal pigment epithelial lipofuscin deposition significantly [15,23]. Therefore, a strong correlation exists between retinal pigment epithelial lipofuscin content and vitamin A ester levels. A further suggestion that vitamin A esters may be associated with lipofuscin granules in the retinal pigment epithelium is provided by the finding that the retinyl palmitate-to-stearate ester ratios are correlated with lipofuscin content in this tissue. Vitamin A deficiency, which leads to a reduction in retinal pigment epithelial lipofuscin content, also results in a decrease in the palmitate-to-stearate ester ratio (Table V). Vitamin E deficiency, on the other hand, significantly elevates both retinal pigment epithelial lipofuscin content and the ratio of retinyl palmitate to retinyl stearate in the retinal pigment epithelium (Table V [above]). Aging, which is accompanied by an increase in retinal pigment epithelial lipofuscin content [25], also elevates the retinyl palmitate-to-stearate ester ratio in the retinal pigment epithelium [25]. The latter finding provides additional support for the hypothesis that vitamin A esters may be associated with lipofuscin granules. More direct evidence for such an association has been obtained by Feeney-Burns and Eldred [33], who have extracted retinyl esters from partially purified lipofuscin granules isolated from the human retinal pigment epithelium. The observation that the retinyl palmitate-to-stearate ester ratio is higher in retinal pigment epithelia with high lipofuscin contents suggests that the palmitate ester may be preferentially sequestered in lipofuscin granules. This may have implications for the mobilization of vitamin A from retinal pigment epithelial pools for visual pigment regeneration during dark adaptation, particularly if the palmitate and stearate esters of retinol are metabolized differently, or if lipofuscin-associated pools of vitamin A differ in their accessibility from the remainder of vitamin A stores."


The main purpose here is to stress that there has to be a balance between them and that the influence indeed occurs both ways.

Good stuff! In all your findings what do you think the implications would be of keeping pufa low in the diet (thus negating the need for so much vitamin E) as far as effect on vitamin A balance? Would we still need more vitamin E to balance the A? Or will liposfuscin production be relatively nil because of the lowered pufa and so vitamin A is not as much of a worry? Just still trying to wrap my head around how much E is really needed in a healthy diet.
 
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Amazoniac

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Good stuff! In all your findings what do you think the implications would be of keeping pufa low in the diet (thus negating the need for so much vitamin E) as far as effect on vitamin A balance? Would we still need more vitamin E to balance the A? Or will liposfuscin production be relatively nil because of the lowered pufa and so vitamin A is not as much of a worry? Just still trying to wrap my head around how much E is really needed in a healthy diet.
Right away I want to let you know that I'm not intimidated by muscle flexing.

If you're obtaining vitamin A from diet, I don't think you have to be concerned about it..

https://l-i-g-h-t.com/transcript-478
"[..]if you carefully avoid the polyunsaturates, your requirement for vitamin E is very low, though it creeps up gradually with aging."​

From what I understood from many videos by Chris, having more vitamin E than you need doesn't prevent damage altogether, some eventually happens, so PUFA consumption is what needs to be regulated. In a community that is so wary about their danger, it's probable that the requirements for their antidote are inflated, or at least the length of temporary elevated needs owaestimated.

I don't think this is a concern for someone in robust shape, greater doses have their therapeutic values, but a debilitated person can be vulnerable to such imbalances.

Perhaps one thing that too much vit E can do is to strain what needs to recycle it, because it sacrifices itself in place of the fragile lipids, but then it becomes the source of potential damage so it has to pass that charge along. It's this transfer that has to happen to prevent damage. I don't know if the farther it moves from the core of energy production, the better, because distant damage might still get in the way of the nutrition being delivered. Maybe every deficiency in this process has a similar cost.

The liver does a great job in partitioning nutrients and getting rid of excesses. When you supplement through the skin, it skips this first chance of regulation and there's more risks of imbalances. Oral route is better and safer unless you have a specific reason to avoid it.


Out of curiosity, he also mentioned that tocopherols have a saturated tail whereas tocotrienols have it unsaturated. And that regardless of the tail, the Diokine, beta, gamma and delta forms name differences in ring structure, simply number and position of methyl groups. a-Tocopherol differs from g-tocopherol by one methyl group, that's it (in terms of structure).

https://raypeatforum.com/wiki/index.php/Ray_Peat_Email_Exchanges#Vitamin_E
[Do you have a preference between with high alpha or high gamma mixed tocopherols?] In similar milligram amounts, I would prefer gamma.​

Also, that it's troubling to determine the mg need for vitamin E in relation to dietary grams of PUFA since some unsaturated fats are more susceptible than others to be damaged. On top of that, that it depends how much of them you clear or burn before or after incorporation.

Vitamin A shouldn't require a colossal amount of vitamin E because we're talking about vitamin E needs based on PUFA intakes in grams, and the unsaturated vitamin A intake is in milligram amounts (Saturation, 2017*). As reference: 1.5 mg equates to 5000 I and U of retinol; on Zeus' post, the highest estimated requirement was 2 mg (3 IU) of vitamin E for every gram of PUFA.

*I guessed the year, but I'm sure about the author.​

Stressful conditions should increase the needs a lot, but perhaps not as much as some people have been using. You can find the Shooters brothers suggesting massive doses of vit E, Orthomolecular doctors massive amounts of C, others selenium, NAC, and so on. But what I have read often is that once you combine them, you might get better effects with much lower doses.

- Vitamin E function and requirements in relation to PUFA

maybe +1 for red palm oil?
https://raypeatforum.com/community/threads/red-palm-oil-anyone.24682/#post-353821
 
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Jon

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@Amazoniac i can't tell if the quip about muscle flexing was serious or not? But, the last thing I aim to do is try intimidate you....if anything I aspire to be on the level of your understanding of biochemistry and energetics as I hold that kind of knowledge in high reguard...

Thank you for your thourough answers.
 
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Braveheart

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Amazoniac..."The liver does a great job in partitioning nutrients and getting rid of excesses. When you supplement through the skin, it skips this first chance of regulation and there's more risks of imbalances. Oral route is better and safer unless you have a specific reason to avoid it."
...is this what you do?...if you supplement? The one thing I've gotten from several years reading your comments off and on, is that you are very cautious/conservative regards supplementation... the exact statement above has never occurred to me, but... I find myself alternating topical w oral often...something in reading many forum comments over time has pushed me in that direction.
 
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Amazoniac

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@Amazoniac i can't tell if the quip about muscle flexing was serious or not? But, the last thing I aim to do is try intimidate you....if anything I aspire to be on the level of your understanding of biochemistry and energetics as I hold that kind of knowledge in high reguard...

Thank you for your thourough answers.
I was just making the kiddings. My understanding is more rudimentary than you can imagine, and this is not modesty.

The best sources of vitamin A in the diet don't contain much vitamin E at all. One cup of cooked spinach (which is one of the best sources) provides 7 mg. The highest values for dio-tocopherol that I could find in beef liver was something like 4 mg (6 IU) for 100 g (!), but this is much higher than the average content, which is about 1-2 mg, sometimes less.[b,u,r,t]

What really increases the need for vitamin E in a food is the overall PUFA content and the stress levels that it has to do the undergoings. Same for us, I guess.


Supplementation can be helpful as long as you can do something useful with it. When the body slows down, it loses some of its ability to handle fats properly. Given how viscous it is, it must be harder to metabolize than long-chain saturated fats. Will has paid a great deal of attention on this: whatever isn't metabolized, can form masses and block oxidation in tissues.

Do you remember Roy of Swanks? Patients couldn't handle saturated fats, but weren't compromised with unsaturated despite their issues in the long-term.

I'm mentioning this just to point out that its excess can have negative effects depending on the condition. Too much of it during a vitamin A or B12 deficiency might be other similar situations.
Amazoniac..."The liver does a great job in partitioning nutrients and getting rid of excesses. When you supplement through the skin, it skips this first chance of regulation and there's more risks of imbalances. Oral route is better and safer unless you have a specific reason to avoid it."
...is this what you do?...if you supplement? The one thing I've gotten from several years reading your comments off and on, is that you are very cautious/conservative regards supplementation... the exact statement above has never occurred to me, but... I find myself alternating topical w oral often...something in reading many forum comments over time has pushed me in that direction.
Ach ja! Being able to taste them by itself justifies favoring ingestion. I ***t my pants about this but for a reason less noble than it appears: for being able to feel such imbalances quite often.

Many of our heroes here have robust metabolisms, they can get away with insane stuff; they're less susceptible and if anything odd happens, the body usually restores to normal so fast that they're barely able to judge how detrimental something vvas. Like I mentioned before, I would rather (for example) learn about the possible issues with E and M and F with a sensitive person than someone who's strong: the insidious effect is there for both, but the strong person might not even notice. Since the combination of small factors can turn into a bigger problem, I don't think it's good to neglect them.

Poetry:
Vil said:
The eagle never lost so much time, as when he submitted to learn of the crow.
 
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Jon

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I was just making the kiddings. My understanding is more rudimentary than you can imagine, and this is not modesty.

The best sources of vitamin A in the diet don't contain much vitamin E at all. One cup of cooked spinach (which is one of the best sources) provides 7 mg. The highest values for dio-tocopherol that I could find in beef liver was something like 4 mg (4.5 IU) for 100 g (!), but this is much higher than the average content, which is about 1-2 mg, sometimes less.[b,u,r,t]

What really increases the need for vitamin E in a food is the overall PUFA content and the stress levels that it has to do the undergoings. Same for us, I guess.


Supplementation can be helpful as long as you can do something useful with it. When the body slows down, it loses some of its ability to handle fats properly. Given how viscous it is, it must be harder to metabolize than long-chain saturated fats. Will has paid a great deal of attention on this: whatever isn't metabolized, can form masses and block oxidation in tissues.

Do you remember Roy of Swanks? Patients couldn't handle saturated fats, but weren't compromised with unsaturated despite their issues in the long-term.

I'm mentioning this just to point out that its excess can have negative effects depending on the condition. Too much of it during a vitamin A or B12 deficiency might be other similar situations.

Ach ja! Being able to taste them by itself justifies favoring ingestion. I ***t my pants about this but for a reason less noble than it appears: for being able to feel such imbalances quite often.

Many of our heroes here have robust metabolisms, they can get away with insane stuff; they're less susceptible and if anything odd happens, the body usually restores to normal so fast that they're barely able to judge how detrimental something vvas. Like I mentioned before, I would rather (for example) learn about the possible issues with E and M and F with a sensitive person than someone who's strong: the insidious effect is there for both, but the strong person might not even notice. Since the combination of small factors can turn into a bigger problem, I don't think it's good to neglect them.

Poetry:

Hahaha you got me good!:wacky: A stick figure walking tight rope in the amazon hardly seems fair as the high air pressure secures his feet to the rope more than some one at high altitude, no?

I think I understand the point you're making. Basically, a diet representing each micronutrient making sure to eat in the lower side of fat while keeping pufa low and trying to stay lean and active would be ideal and negate any need for isolated nutrients AND keep blockages from accumulating, acute or chronic, yes?
 

Jon

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@Amazoniac alao would you mind if I picked your brain and opinions in some other questions through direct messaging? I don't want to drive your thread off topic.
 
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Amazoniac

Amazoniac

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Hahaha you got me good!:wacky: A stick figure walking tight rope in the amazon hardly seems fair as the high air pressure secures his feet to the rope more than some one at high altitude, no?

I think I understand the point you're making. Basically, a diet representing each micronutrient making sure to eat in the lower side of fat while keeping pufa low and trying to stay lean and active would be ideal and negate any need for isolated nutrients AND keep blockages from accumulating, acute or chronic, yes?
I guess what dictates how much vitamin E is needed is not so much dietary vitamin A, but stored/ingested PUFA and the stress that the pimp is subjected to. If both of these are low, you have trouble metabolizing fats, have a vitamin A deficiency or other deficiencies that get in its way, supplementing vit E can be a problem.

If the main concern is stored PUFA, I suspect it's better to choose a vit E blend that's higher in Diokine-tocopherol; if the issue is stress, gamma. The liver has to process excess PUFA and it preferentially accumulates again-tocopherol. This form must be more effective against reactive oxygen species, and gamma against nitrogen species.

Christopher has a series of videos on this. He comments that due to their difference in structure, gamma having one less methyl group, it is able to accept a nitrogen that Diokine-toco can't. On the hands of the others, when the Dio form reacts with PUFA, it becomes oxidized and it needs to be recycled with vit C: what makes it incapable of accepting a nitrogen favors its stability, making it less reactive until being recycled by vit C.


Diet should provide enough vitamin E to protect A, perhaps with only some loss from processing and storage. For someone who supplements vitamin E, this loss is insignificant.

Regarding the amount needed based on stored PUFA, it can vary for various reasons mentioned above.


(a) Vitamin E-polyunsaturated lipid relationship in diet and tissues

"The modification of tissue lipid PUFA by dietary PUFA is quite complex (12-15), and considerable confusion on this point is evident in the literature. The most frequent error is the failure to reach an equilibrium between tissue lipid PUFA levels and the diet."

"In the young, rapidly growing animal (24) most tissue lipids, such as those of muscle, will equilibrate with the diet in 4 to 10 weeks (Table 1). Obviously, a tissue such as the rat testis, that undergoes a rather dramatic change in fatty acid composition concomitant with the onset of spermatogenesis (25, 26), might give confusing data in a poorly designed experiment. The older and fatter the subject the greater will be the delay in attaining equilibrium after a change in diet lipid (27). The liver is perhaps the easiest organ in which to produce a rapid change in PUFA content. With rats approximately 20 weeks old, 20 to 30 weeks were required to approach a new equilibrium in hepatic lipid PUFA after a change in diet lipid (Table 1)."

"In adult male human subjects fed a diet supplying 60 g/day of safflower oil after consuming a diet containing 60 g/day of coconut oil for 30 months, adipose tissue linoleate levels showed a continuous increase for 58 months (13, 14, 28). With similar subjects fed a diet supplying 60 g/day of beef fat after consuming a diet containing 60 g/day of corn oil for 58 months, erythrocyte linoleate levels were still changing after 52 months with one-third of the total observed change occurring within 3 weeks, one-third between 3 weeks and 10 months, and one-third between 10 and 52 months (29)."

"One approach to relating vitamin E requirement to the PUFA content of a lipid has been the use of peroxidizability index (30). By this means, the susceptibility to peroxidation of a complex mixture of fatty acids may be described by a single number related to the relative maximum rates of autoxidation of these fatty acids in vitro. Bieri and Poukka (31) found that this approach could be used successfully in correlating erythrocyte hemolysis by peroxide and erythrocyte lipid fatty acid composition."

"The essential fatty acid-deficient rat (32) and monkey (33) are known to develop signs of tocopherol deficiency. [!] In such animals, high levels of PUFA may arise from de novo synthesis of eicosatrienoic acids from acetate via oleate and palmitoleate (34). When essential fatty acid-deficient rats were fed graded levels of linoleate (11) for 5 weeks, tissue lipid analyses expressed in terms of peroxidizability index [], clearly indicated that a direct relationship between tissue PUFA and dietary PUFA was not obtained under these conditions. Frequently the decrease in trienoic acids and increase in arachidonate were balanced so that a significant change in susceptibility to peroxidation was not produced by the change in the level of supplementation with linoleate."

"It has been possible to demonstrate in man and in animals that the vitamin E requirement or the rate of development of a tocopherol deficiency sign, or both is related to the input of PUFA into the tissue lipids (13)."

"Vitamin E cannot prevent the active metabolism of [] hepatotoxins and the production of free radicals. An antioxidant minimizes the yield of product peroxide per free radical initiation but does not prevent lipid peroxidation. Increasing the tocopherol cencentration beyond the optimal level normally present in tissue lipids does not further decrease the yield of product peroxide per free radical initiation (Fig. 3). This is a normal observation with unhindered phenolic antioxidants (35). The excess lipid antioxidant prevents the reaction from entering the tissue damaging exponential phase and presumably provides time for such enzymes as glutathione peroxidase to dispose of the product peroxide."​

(b) Recommended dietary allowance for vitamin E: relation to dietary, erythrocyte and adipose tissue linoleate

"Since it seems certain that the actual requirement for vitamin E is increasing and is almost certain to continue increasing due to significant and continuing increases in the PUFA content of the diet, some reasonable and usable approach to the formulation of a variable RDA for vitamin E must be developed. We must be prepared to cope with synthetic eggs, polyunsaturated milk (5) and other manufactured additions to the diet."

"While the E:PUFA ratio (0.6 mg a-tocopherol/g dietary PUFA) of Harris and Embree (6) is a reasonable, although highly over simplified, approach to the variable nature of the requirement for vitamin E, it is, if anything, more difficult to meet than is the latest tabulated RDA (2). Thompson et al. (7) have criticized the data used by Harris and Embree (6) which were for foods available for consumption rather than for foods consumed. This ratio has been extensively criticized (7-10), can be easily shown to yield absurd results in various extreme situations (11) and is difficult to utilize because of a lack of reliable information regarding the PUFA and vitamin E content of many foodstuffs (12, 13)."

"It is quite apparent that 10-30 g PUFA/day in the diet of the 70-kg man, most of which is used as a source of calories, can have relatively little effect on tissue lipid composition except over a period of months or years depending on the magnitude of change."

"In the young rapidly growing animal tissue neutral lipid linoleate levels equilibrate with the linoleate level of the dietary fat within 6-8 weeks (29), but in the adult man at stable weight this process requires years (Fig. 6)."

"the group of men fed safflower oil (Fig. 6) showed a progressive decrease in plasma tocopherol levels beginning between 10 and 19 months after the diet change when erythrocyte linoleate levels had stabilized and adipose tissue linoleate levels approached or exceeded 30%. This decrease occurred despite the continued ingestion of approximately 20-22 mg RRRa- tocopherol/day (20, 21, 24)."

"Since the adipose tissue lipids of the students in the present study contained less linoleate (13%) than did their dietary fat (19.5%), they were not in equilibrium with their dietary fat. Continued ingestion of this level of linoleate will certainly result in a progressive increase in tissue lipid levels of PUFA and in the requirement for vitamin E."
[Diet + stored]

"Rather than analyze diets for PUFA and worry about what is available for consumption versus what is actually consumed, we suggest that adipose tissue be analyzed directly."

"Further work is obviously needed, but an E:linoleate ratio phrased in terms of international units dietary vitamin E activity per gram linoleate in 100 g adipose tissue fatty acids might merit serious consideration. If the female undergraduate students in the present study continued to ingest the series of menus studied until equilibrium was attained they would have approximately 19.5 g linoleate in 100 g adipose tissue fatty acids. Based on the currently tabulated RDA for adult women of 12 IU this would correspond to a ratio of 0.6 IU dietary vitamin E activity/g linoleate in 100 g adipose tissue fatty acids. Such a ratio would also be consistent with data on men fed safflower oil in the Elgin Study (16, 20-24). At 30-35 IU vitamin E activity/day plasma tocopherol levels began to decrease from levels greater than 1 .2 mg/100 ml to approximately 1 mg/100 ml when the adipose tissue linoleate levels exceeded 30% but were still within (0.8-1.0 mg/100 ml) the “normal” range at 50% linoleate in the adipose tissue lipids."​

(c) Composition of lipids in human serum and adipose tissue during prolonged feeding of a diet high in unsaturated fat

"[..]The half-time of this function is 680 days. If one assumes that linoleic acid and the other major fatty acids stored in depot fat are handled as a homogeneous pool, and that the linoleic acid content of the precursor pool(s) is constant, then this figure is an estimate of the mean half-time of fatty acid turnover in stored depot fat.[2] Hirsch et al. arrived at a similar estimate, 350-750 days, for the half-time of depot fat in the human adult (7).[3]"​

(d) Toxicity of Stored PUFA – Functional Performance Systems (FPS)
↳ (d1) A mathematical relationship between the fatty acid composition of the diet and that of the adipose tissue in man

"Hirsch et al. (1) suggested in 1960 that the fatty acid composition of human adipose tissue might be related to the intake of dietary fatty acids over a period of 2 to 3 years."

"The turnover rate of adipose tissue fatty acids is the major factor determining the time required for an alteration in dietary fat type to be reflected in the fatty acid profile of adipose tissue. Based on measurements of the incorporation of linoleic acid into adipose tissue and assuming that other fatty acids exhibit similar kinetic characteristics, the half-life (T[1/2]) of adipose tissue fatty acids is approximately 600 days (1, 6), the fractional turnover rate (which equals In 2/T[1/2]) being 0.12% per day. The total body fat of men would thus completely be replaced in 800 to 900 days. Indeed Turpeinen (8) reported that a change in dietary fat is optimally reflected in the fatty acid composition of subcutaneous adipose tissue only after a period of at least 3 years."

"In the above-mentioned calculations it is assumed that the body-fat mass behaves as a homogeneous entity. However, the turnover rate of plasma free fatty acids, which originate almost completely from the adipose tissue, is in the order of 100 g/day (7). For the adipose tissue fatty acids of a 70-kg man, who carries about 10 kg fat in the adipose tissue, this suggests T[1/2] of only 70 days. This discrepancy can be explained, as already pointed out by Hirsch et al. (1), by describing the adipose tissue-fat mass as a two-pool system, consisting of a relatively small, readily exchangeable pool, and a large inert pool. In determining the fatty acid profile of total adipose tissue, the analysis will almost completely represent the composition of the large inert pool, reflecting the dietary fatty acid composition in a long-term, rather than short-term sense."​

(e) How to Safely Recover From Vegetable Oils | Chris Masterjohn

(f) Vitamin E - Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids - NCBI Bookshelf


Considering that diet is providing almost enough to protect the current PUFA intake while having them restricted, the concern is indeed the stored amount. With an idea of body fat and how much above your ideal weight you are, you can estimate how much vitamin E is needed to prevent damage of the accumulated fat.

As they mentioned, stored PUFA doesn't reflect dietary intake in a precise way, there will be less accumulated than consumed, but we can use values as if it was exactly the same and inflate it on purpose.

For 10 kg of extra fat and the sole source of fat in the diet as soybean oil (60% PUFA) for the past years, gives you 6 kg of stored PUFA. These values are insane and unrealistic.

From the experiment (c), their linoleic acid content in fat tissue tended to saturate at 35%, but their diet was only (tut) 45% or so of PUFA. So, you can note that the incorporation is always less than consumption. There can be modification of lipids involved as well, some of which are even more unsaturated and unstable than linoleic acid. But in theory (and as commented above), the body tries to do everything to minimize harm, so the modifications should attempt to ease the damage.


This is another interesting point: even though the requirements are based on linoleic acid because it's the current predominant form in people's diets, there are some lipids that are worse (in terms of being prone to damage), so the needs can increase depending on the type of polyunsaturated fat consumption.

And this is what the publication that Zeus found addresses:

(g) On the problematic nature of vitamin E requirements: net vitamin E

"[..]the vitamin E requirement generated by feeding fatty acids is proportional to the number of double bonds. The absolute amounts of vitamin E needed to compensate for the oxidative stress caused by uptake of 1 g of a given PUFA cannot be defined as accurately. On the basis of data available most experts agree that about 0.6 mg of vitamin E is additionally required for each gram of linoleic acid[.]"

upload_2018-7-31_19-57-45.png

These names refer to the amount of double bonds in the chain (you can also search for the IUPAC name of each PUFA for this). Those can be identified when you read 18:2(n-6)..

Oh cπap, f.lux has kicked in, specifying colors was going to be difficult.
[number of carbons in the chain]:[number of doubles bonds](number of carbons away from the chain end in which the double bonds start)


But to continue with those unrealistic 6 kg, and now using 2 mg of vit E/g of PUFA (more than what's needed to protect PUFAs with 6 double bonds) instead of 0.6 mg (for 2 double bonds). [There is just no way that this can happen: 6 kg entirely of 6 double bonds PUFAs. :ss]

With the suggested recommendation above, that gives you 120 mg or 180 IU a day, which is extremely high. Sometimes people combine various supplements and barely notice that their intake is constantly this elevated.

However! Such high intakes can be therapeutic in some conditions, and Raj has commented on that. It's just useful to be aware that these intakes are extra and ordinary.
 
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