Low Toxin Diet Grant Genereux's Theory Of Vitamin A Toxicity

[InChristAlone]

No, but perhaps the obesity is protective.

There are dozens of studies showing that lower serum retinol has a higher likelihood of cancer.

There are dozens of studies showing that RBP4 causes insulin resistance and obesity.

I'm not proposing this as a hypothesis, just throwing some ideas out.

Yeah well one of my early concerns with Grant was the lower cholesterol and whether he will get cancer someday, but honestly his quality of life seems loads better than it was before and he has no signs of kidney disease anymore, that's huge. Cancer is a whole 'nother beast, but if we believe cancer is a cell metabolism thing then he isn't showing much sign of being headed that way other than the lower cholesterol and pulse.

 

[Blossom]

Yeah well one of my early concerns with Grant was the lower cholesterol and whether he will get cancer someday, but honestly his quality of life seems loads better than it was before and he has no signs of kidney disease anymore, that's huge. Cancer is a whole 'nother beast, but if we believe cancer is a cell metabolism thing then he isn't showing much sign of being headed that way other than the lower cholesterol and pulse.

Cholesterol is so misunderstood and the pharmaceutical industry didn’t do us any favors.
Grant seems like a pretty intelligent and capable guy so I’m hopeful he will be able stay on top of things in regards to his health.
I’m personally going to keep my cholesterol monitored because it’s already gone down significantly (total by 80 points!).
This cholesterol confusion has been plaguing me for ten years now. I do think it can definitely be impacted by inflammation and if your not inflamed you probably don’t need to produce so much. I also think there is a small group of people that have an inherited tendency to produce more than optimal. Otherwise I think there is probably a wide range in what can actually be healthy and it seems to vary between different people and within an individual depending on how much they need according to their current state. He wrote a good blog post on cholesterol recently. I do wonder if the correlation with cancer isn’t misunderstood stood and yet again cholesterol is just an innocent bystander at the scene of the crime. All of this is just my layman speculation and musings.

 

[InChristAlone]

Cholesterol is so misunderstood and the pharmaceutical industry didn’t do us any favors.
Grant seems like a pretty intelligent and capable guy so I’m hopeful he will be able stay on top of things in regards to his health.
I’m personally going to keep my cholesterol monitored because it’s already gone down significantly (total by 80 points!).
This cholesterol confusion has been plaguing me for ten years now. I do think it can definitely be impacted by inflammation and if your not inflamed you probably don’t need to produce so much. I also think there is a small group of people that have an inherited tendency to produce more than optimal. Otherwise I think there is probably a wide range in what can actually be healthy and it seems to vary between different people and within an individual depending on how much they need according to their current state. He wrote a good blog post on cholesterol recently. I do wonder if the correlation with cancer isn’t misunderstood stood and yet again cholesterol is just an innocent bystander at the scene of the crime. All of this is just my layman speculation and musings.

Yeah I bet we wouldn't need so much cholesterol if there isn't as much inflammation. And I totally believe it is just the innocent bystander keeping people alive. My cholesterol went up on the Peat diet. It went down by about 10 changing things up but I was still eating liver once a month or two last I tested. I'll be interested to see what my numbers look like next year.My husband was never into eating liver and he also probably has a much bigger liver than I do and his cholesterol has stayed lower than mine.

 

[InChristAlone]

I just remembered something! There is a well known Ray Peat practitioner who regularly recommended vitamin A to people as long as they balanced it with D, well he said sometimes he would take large doses of it in the summertime. He ended up in the hospital with near kidney failure a few years ago. Well so he says, no one confirmed this was true. I am not sure if he continued using vitamin A, but there are a lot of questions!

I am loving the testimonials on this thread saying their outlook on life is so much better! I was reminded of this because of a quote by Ray Peat regarding using a very large dose to keep away acne and leukoplakia. It is quotes like that, that have gotten people in trouble in this community. As Amazoniac was showing us the size of someone's liver varies greatly. Maybe Ray Peat has a very large liver!!!

 

[Amazoniac]

It's quite concerning that depleted animals do not store their vitamin A properly, in the liver. That is a paradox for anyone embarking on vitamin A depletion as a means to heal themselves. It means that depletion might be ultimately self-defeating.

It's hard to make sense of that phenomena for something that's supposed to be absolutely essential. There's still so many unknowns...
How is Grant not breaking down after 4.5 years?
I was pleased to see @Amazoniac's posts about estimated time for depletion earlier in the thread.

It took a good while for me to understand a meaning of maladaptation:
- NAD/NADH Ratio - The One Metabolic Cause To Rule Them All

In wondering..

Will (Gehard, 1998) or wow is poison/"vitamin" A?​

..I guess it's worth commenting that even though blood level of poison A is unreliable when it's higher (the depletion or excess in some persons can be marked but blood levels appear fine), when it drops below 10 mcg/dl(100 ml) there are authors who claim that the association with liver reserving less than '10 mcg poison/g tissue' is invariable. This stage is often beyond symptoms, the signs start to appear.

While many aspects of the experiment below were not right (estimation of liver stores for example were off), a more reliable one was the length that it took to deplete each subyect; they was being carefully examined, and they only begun repleting them when they judged it was needed.

It took at least a year, but in some more than 2 years. Their electroretinograms were abby normal (gina, 2018) before there were changes in dark adaptation, which in turn happened in all subjects after 8-15 months. All of them also experienced thickening of the outer layer of skin and some reported other issues as well. Of course these are early consequences and the researchers terminated the depletion phase before anything had chance to advance. And we don't know what gets compromised without being perceptible.

Chickity-check yo self before you wreck yo self (Cube, 1993; Graham, 1998) going over the boards:

- Vitamin A Metabolism and Requirements in the Human Studied with the Use of Labeled Retinol

Spoiler

"The subjects were fed the various types of diets indicated in Table V. Diets I-IV were virtually devoid of vitamin A and carotenes. In all other respects, the diets were considered adequate. Diet I was a vitamin-free casein liquid formula similar to that used previously by Hodges ef al. (1971). The subjects consumed approxirnately 15% of their calories from protein, 40% from fat, and 45% from carbohydrates. Diets I-A, I-B, and I-C represented only modifications in the fat sources in the diets to eliminate traces of vitamin A. Diet II represented a solid diet of soy protein products. Diet III represented a combination of the casein formula diet and the soy protein diet to provide a reduced intake of vitamin A. Diet IV represented a modification of the menus employed in the Sheffield study [by Hume and Krebs, posted before; check out the equipment that they had at their disposal]. The dietary contribution of vitamin A thoughout the study was exceeding low and the cooperation of the subjects was excellent. The diets were constantly monitored and analyzed throughout the study." "The subjects were maintained on the experimental diets for periods up to 854 days [!] (Table IV)."

"Physical examinations were conducted daily. Because of the nature of the investigation, extensive ophthalmological measurements were performed. Tests conducted at least once every month throughout the study were dark adaptometry, electroretinography, electro-oculography, visual acuity, and macular fatigue. Information was also obtained during the study on intraoccular pressure, and color vision. Changes in taste, smell and vestibular function, cerebrospinal fluid pressure, and plasma retinol binding protein levels were also measured."

"When diet II was fed (for the next 63 days), it soon became apparent that the plasma levcls were rising somewhat. The reason for this change was not clear and may have representcd either a physiological adjustment to the condition of vitamin A depletion or a response to the change in diet. Although diet II contributed only 23 mcg of retinol per day to each subject, subsequent repletion results obtained in the study would suggest that this small contribution of vitamin A should have had only a negligible effect on the vitamin A plasma level and on the depletion process. Moreover, the radiometric data [] did not reveal any apparent change in plasma retinol specific activity or in depletion of body vitamin A pools."

They were all wealthy from the start, so their internal consumption was probably greater than a turtled person. Taking way more than that to deplete must still be possible, and might be the case of the guru.

In fever, poison A is used up faster, so if a person has high metabolic rate, it's a constant revef-like state.


I forgot to comment that the consequences of owa or underestimations of certain individuals (what was being discussed with Blossom) will affect the end of their calculation by changing the adjustment for variation (which can be a lot); since the values will be more dispersed, it forces them to push requirements higher to make sure that most people will be covered.

All in the all, I don't think it matters much because they're being conservative for thinking in terms of minimum required to maintain a desirable level and suggesting an amount needed for this; there must be a range in which the body has no problems in regulating and what they're (in theory) proposing is the lower side of it. It shouldn't be a matter of crossing from dearth (that eventually leads to depletion) to excess (with accumulation and eventual toxicity) without passing first through a safe transitioning range. So it's likely that we has some thousands of IU of acceptable deviation that's still within the optimal range and the body won't have problems disposing what's not needed. Which is why if this is not oper and ating, it suggests that others issues might be at the play.


- Grant Genereux's Theory Of Vitamin A Toxicity
- Grant Genereux's Theory Of Vitamin A Toxicity
- Grant Genereux's Theory Of Vitamin A Toxicity
- Grant Genereux's Theory Of Vitamin A Toxicity
- Grant Genereux's Theory Of Vitamin A Toxicity

 

[Orion]

"The subjects were fed the various types of diets indicated in Table V. Diets I-IV were virtually devoid of vitamin A and carotenes. In all other respects, the diets were considered adequate. Diet I was a vitamin-free casein liquid formula similar to that used previously by Hodges ef al. (1971). The subjects consumed approxirnately 15% of their calories from protein, 40% from fat, and 45% from carbohydrates. Diets I-A, I-B, and I-C represented only modifications in the fat sources in the diets to eliminate traces of vitamin A. Diet II represented a solid diet of soy protein products. Diet III represented a combination of the casein formula diet and the soy protein diet to provide a reduced intake of vitamin A. Diet IV represented a modification of the menus employed in the Sheffield study [by Hume and Krebs, posted before; check out the equipment that they had at their disposal]. The dietary contribution of vitamin A thoughout the study was exceeding low and the cooperation of the subjects was excellent. The diets were constantly monitored and analyzed throughout the study." "The subjects were maintained on the experimental diets for periods up to 854 days [!] (Table IV)."

Granted showed that the studies using casein in the earlier labs, was actually giving the rats high dose retinoic acid. Retinol is bound in casein, heating it to clean and pasteurize it produces retinoic acid, so they where essentially on accutane. How did the researchers conclude that the casein was vitamin A free?

 

[Amazoniac]

Granted showed that the studies using casein in the earlier labs, was actually giving the rats high dose retinoic acid. Retinol is bound in casein, heating it to clean and pasteurize it produces retinoic acid, so they where essentially on accutane. How did the researchers conclude that the casein was vitamin A free?

Orion! It doesn't explain the bump from the soy protein diet or their combination that continued the drop, I guess retinoic acid could spare blood levels somehow. You're suggesting that people were stressed by it during the entire experiment, but what's the most likely explanation here? I suppose they remove the fat first and only then sterilize it. If this is the case, only trace amounts are left present and shouldn't be a big deal. Removing these impurities might shorten the time needed to deplete and reinforce our concern.

 

[Orion]

Orion! It doesn't explain the bump from the soy protein diet or their combination that continued the drop, I guess retinoic acid could spare blood levels somehow. You're suggesting that people were stressed by it during the entire experiment, but what's the most likely explanation here? I suppose they remove the fat first and only then sterilize it. If this is the case, only trace amounts are left present and shouldn't be a big deal. Removing these impurities might shorten the time needed to deplete and reinforce our concern.

I would say I don't trust that the all the diets were vitamin A free, like the botched experiments in the 1920 and 30. What year was the study performed?

 

[Amazoniac]

I would say I don't trust that the all the diets were vitamin A free, like the botched experiments in the 1920 and 30. What year was the study performed?

I think around 1972.

 

[Orion]

I think around 1972.

Do you have access to the way they prepared the casein and tested it for for all types vitamin A?

It says that diet II has 23ug retinol per day, was the soy flour oxidized, again introducing retinoic acid(accutane)?

Soy beans per 100g
Vitamin A 180.00 IU 4 %
Vitamin A, RAE 9.00 mcg

 

[Tarmander]

Grant's experience is surprising, but so is how the current RDA was defined. You might be just as surprised if you haven't check it out yet.

- Recommended dietary intakes (RDI) of vitamin A in humans

"The structural requirements for the biological activity of vitamin A are generally very strict: for example, the growth-promoting activity of vitamin A is reduced or eliminated by isomerization of the double-bond system, lengthening or shortening of the central chain, oxidation of the trimethyl-cyclohexene ring, and removal of the methyl groups (4). The same structural requirements apply to the carotenoids. Thus, of more than 500 carotenoids found naturally, only about 50 have provitamin A activity (3, 5,6)."

"In food, preformed vitamin A is present mainly as retinyl ester. In the stomach retinyl esters and various carotenoids are released from the food by proteolytic activity and then aggregate into globules with other dietary lipids. In the intestine retinyl esters are hydrolyzed, and the products are associated first with lipid globules and then with bile salt-containing micelles in the intestinal lumen. Both vitamin A and carotenoids are absorbed best in the upper part of the small intestine; absorption efficiency decreases lower in the gut. The absorption of retinol and b-carotene also differs in several ways:

1. In physiological amounts retinol is more efficiently absorbed than are carotenoids; eg, 70-90% vs 20-50% (7, 10).
2. As the amount ingested increases, the efficiency of retinol absorption remains high (60-80%) whereas that of carotenoid absorption falls markedly (< 10%) (7, 11).
3. Retinol is well absorbed from a micelle formed either with bile salts or with nonionic detergents, such as polyoxyethylene sorbitan derivatives, whereas carotenoids are absorbed in the presence of bile salts but not of nonionic detergents alone (12, 13). Indeed, the structure of the bile salts present affects the absorption of both vitamin A and carotenoids (12, 13).
4. At low physiological intakes, ie, 20-200 nM in lumen fluid, vitamin A is transported across the intestinal cell membranes by a carrier-mediated process (12, 14) whereas carotenoid absorption seems to occur by diffusion from a micellar phase. At high concentrations, vitamin A also seems to diffuse into intestinal cells through a micellar phase."

"Absorbed retinol is largely esterified with palmitic acid in intestinal mucosal cells and incorporated into the lipid phase of chylomicrons. b-carotene and other biologically active carotenoids are cleaved in the cytoplasm of intestinal cells to retinaldehyde, which is reduced mainly to retinol and then esterified to retinyl palmitate and other similar esters. Some carotenoids are incorporated directly into chylomicrons and some retinaldehyde is oxidized to retinoic acid."

"Chylomicrons, which contain uncleaved carotenoids and most of their vitamin A in ester linkage, pass first into the lymph and then into the systemic circulation. They are then converted rapidly by the action of lipoprotein lipase to chylomicron remnants, which are taken up mainly by hepatocytes in the liver (15). When initial liver reserves of poison/"vitamin" A are low, part ofthe newly absorbed vitamin A is released into the blood as a 1:1 complex with plasma retinol-binding protein (RBP) and part is stored as retinyl ester in hepatocytes (15, 16) with very little transferred to stellate cells. When liver reserves of vitamin A are adequate (> 20 mcg/g or > 0.07 umol/g), however, much of the newly absorbed vitamin A is transferred to stellate cells of the liver and is stored as retinyl ester (15, 17-19). In well-nourished individuals, the storage efficiency of ingested vitamin A in the liver is > 50% (20) [Values have lowered since the publication]. In contrast, depleted animals store ingested vitamin A poorly (21)."

"Vitamin A is released from the liver as holo-RBP. The RBP in holo-RBP is recognized by surface receptors on target cells, retinol is transferred across the plasmalemma into the cell, and the resultant apo-RBP is modified and released. Modified apo-RBP is removed and hydrolyzed mainly in the kidney (22,23). Approximately 80% of the retinol transported to peripheral target cells is recirculated back to the liver (24-26). The relatively short half-life (11-12 h) of plasma holo-RBP (27, 28) and the extensive recycling of retinol between peripheral tissues and the liver attest to the dynamic homeostatically controlled relationship between blood and these tissues (26)."

"In well-nourished persons, the liver contains >90% of the total-body stores of vitamin A. In poorly or marginally nourished individuals, however, the kidneys as well as other tissues contain an appreciable amount (10-50%) of the total-body reserve of the vitamin."

"Unlike vitamin A, carotenoids are deposited mainly in human adipose tissues; relatively small amounts are stored in the liver. The corpus luteum contains a very high concentration of carotenoids."

"Vitamin A is metabolized in two major ways: by oxidation of the C-4 position of the cyclohexene ring (30) and by oxidation of the C-is position to retinaldehyde and then irreversibly to retinoic acid. Except for vision and in testicular development, retinoic acid is essentially as active biologically as ingested vitamin A. Subsequent events involve oxidative cleavage of the unsaturated carbon chain and conjugation with glucuronic acid or taurine with or without chain cleavage (31, 32). Most of these conjugated polar metabolites are secreted into the bile, and a significant portion (~30%) of retinoyl b-glucuronide is recycled back to the liver in an enterohepatic circulation (31). Of the total vitamin A metabolized, approximately equal amounts appear in the feces and in the urine. Essentially all of these excreted products are modified biologically inactive metabolites of vitamin A; very little intact vitamin A is excreted."

"Because only a few carotenoids serve as provitamin A and because many other yellow and orange pigments are present in plants, the color intensity of a fruit or vegetable is not necessarily a good indicator of its content of propoison A."

"Adequate intakes of vitamin A have been estimated on the basis of the amounts needed 1) to correct impaired dark adaptation among vitamin A-depleted subjects, 2) to raise the concentrations of vitamin A into normal range in the plasma of depleted subjects, and 3) to maintain a given body-pool size of vitamin A in well-nourished subjects."

"Large doses of a-tocopherol [] inhibit b-carotene uptake by the intestine (66)."

"Deficiencies of a variety of other nutrients, including protein, a-tocopherol, iron [coughper], and zinc also adversely affect vitamin A transport, storage, and utilization (3, 6, 24)."

"In large doses vitamin A and other retinoids show dramatic chemopreventive effects in animals against some forms of cancer (2,68,69)."

"Unlike vitamin A, most carotenoids trap free radicals at low oxygen tensions (72) and quench singlet oxygen, which can cause neoplastic changes in cells. Because only ~10% of carotenoids in nature show propoison A activity, however, any anticancer effects that carotenoids possess would seem more properly to be attributed to their rather unique antioxidant properties than to their conversion into poison/"vitamin" A (73). This viewpoint is supported by the recent observation that the ingestion of carrots, which are rich in nutritionally active carotenoids, was not associated with any protection against neoplasm (74), whereas the intake of tomatoes, which mainly contain the nutritionally inactive carotenoid lycopene, was."

"Plasma poison/"vitamin" A values often are not good indicators of total-body reserves even when the latter are low (43, 46). Indeed, Sauberlich et al (20) also reported that two of eight subjects showed fairly high plasma retinol levels even after significant periods of depletion."

"The full recovery of the complex homeostatic system for the control of plasma vitamin A values is slow in fully depleted subjects and usually requires either a long period at moderate doses (20, 40) or single large doses."

"Healthy individuals with adequate liver reserves of vitamin A in many world cultures can show plasma values <30 mcg/dL (<1.05 uM)."

"Infections, drugs, and other forms of stress can transiently lower plasma retinol values below 30 mcg/dL (1.05 uM) without having any apparent effect on vitamin A status."​

- Poison/"vitamin" A | Linus Pauling Institute

"Vitamin A deficiency in animal models was found to interfere with the pituitary-thyroid axis by (1) increasing the synthesis and secretion of thyroid-stimulating hormone (TSH) by the pituitary gland, (2) increasing the size of the thyroid gland, (3) reducing iodine uptake by the thyroid gland and impairing the synthesis and iodination of thyroglobulin, and (4) increasing circulating concentrations of thyroid hormones (reviewed in 51)."​

- Vitamin A concentration in human tissues collected from five areas in the United States

View attachment 12334​

- Vitamin A - Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - NCBI Bookshelf

"Evidence Considered in Estimating the (Adult) Average Requirement

The calculation described below can be used for estimating the vitamin A requirement and is calculated on the basis of the amount of dietary vitamin A required to maintain a given body-pool size in well-nourished subjects. Olson (1987) determined the average requirement of vitamin A by this approach using the calculation:

A × B × C × D × E × F"

A = Percent of body vitamin A stores lost per day when ingesting a vitamin A-free diet

"The portion of body vitamin A stores lost per day has been estimated to be 0.5 percent based on the rate of excretion of radio-activity from radiolabeled vitamin A and by the calculation of the half-life of vitamin A."

In the experiment that served as base, the half-life of stored poison varied a lot. According to their extremes, in one person it took 75 days to deplete the body content in half; in other, 241 days. Of the 8 people being monitored (including those 2), the mean half-life of the reserves was 154 days. If it takes 154 days to deplete 50% of the stores, they assume that 0.32% (50% ÷ 154) is lost a day.

- Vitamin A Metabolism and Requirements in the Human Studied with the Use of Labeled Retinol (posted in this thread before)

View attachment 12326​

There's a different approach to it, but the researcher didn't provide enough details, so it has been tough to get how he arrived at it. I'm not sure if I'll try to work it out, however it doesn't change the rate of depletion because in both they round them to 0.5% like savages.

The percentages above are gross simplifications because it's considering that the process is linear at all times. Yeet! The rate of utilization is high at the beginning and lowers the closer you get to depletion. You might deplete half of your stores relatively fast, but the other half is more difficult; and if you divide the second half in two, the last period lasts longer than the previous, and so on if you continue half-lifeing them.

View attachment 12328​

Either way, in rounding to this higher percentage (0.5%) they is assuming it to be depleted faster, which in turn reflects in recommending higher intakes to replenish what's used/lost daily. But at the same time, unless you remain without ingesting poison for the entire specified half-life, the actual depletion rate in the initial moment might be that great, if not greater than that. Fragmentation of the periods also minimize problems when you consider each of them linear. So these aspects might cancer each other out.

So perhaps it makes sense to use it for practical purposes given that they have regular consumption in the minds. The variation between gurus is still insane, but it will be taken into consideration later on (although by pushing recommendations higher as solution).​

B = Minimum acceptable liver vitamin A reserve

"The minimal acceptable liver reserve is estimated to be 20 μg/g and is based on the concentration at which (1) no clinical signs of a deficiency are observed, (2) adequate plasma retinol concentrations are maintained (Loerch et al., 1979), (3) induced biliary excretion of vitamin A is observed (Hicks et al., 1984), and (4) there is a protection against a vitamin A deficiency for approximately 4 months while the person consumes a vitamin A-deficient diet."

Quoting a part from the previous publication:

"[A] crucial step is the selection of a satisfactory total-body reserve, or more conveniently, a liver vitamin A concentration that prevents deficiency, provides a suitable reserve for periods of stress and/or low intake, and is fully consistent with good health. A liver vitamin A concentration of 20 mcg vitamin A, expressed as retinol, per gram liver (0.07 umol/g) meets the following tests of adequacy:

1. no clinical signs of deficiency have been noted in individuals with this or higher liver concentration;
2. the liver is capable of maintaining steady-state plasma retinol values at this concentration, as determined by the relative dose response test (42, 43), but not at a concentration of < 10 mcg/g liver (<0.035 umol/g);
3. mechanisms for the inactivation and biliary excretion of vitamin A are induced in the liver when liver stores rise significantly above this concentration (44), and[..]
4. this concentration is sufficient to protect an adult ingesting a diet free of vitamin A from a deficiency state for ~4 mo as well as to meet vitamin A needs during shorter periods of stress, such as infection, exposure to extremes of temperature, etc. Furthermore, this liver concentration is used increasingly in the international scientific literature as a reference point of vitamin A adequacy (43, 45-48)."

C = The liver weight:body weight ratio

"The liver weight:body weight ratio is 1:33 (0.03) and is an average of ratios for infants and adults."

When you calculate using their 3% of body weight as suggested above, you end up with livers weighting 2.3 kg for pimps (76 kg) and 1.9 kg for pimpesses (62 kg).

Here are various formulas proposed to estimate liver weight based on body weight:
- Estimating liver weight of adults by body weight and gender

It's based on volume (ml) but they provide a conversion factor: 1.19 ml/g.
Some require surface area, which was already discussed elsewhere.​

They comment that some formulas are better suited for certain populaces. Read the articulo for more information.

But as an example, for a guru that weights those 76 kg and is 175 cm tall, the liver weights [. . . Brewing a random formula . . .] 1.65 kg; which is about 2% of total weight instead.

Now compare our 2% (which is more accurate) with their 3%. 1% might not seem a lot, but it's an assumption that the liver is 50% bigger: a brutal owaestimation of reserves, which ends up increasing the requirement that should provide a minimum desirable amount to maintain adequacy.

One of the reasons for the distortion is their grouping of the proportions for fetuses (4.2%) (their liver weight:body weight ratio is higher) with those for adults (2.4%): (4.2% + 2.4%)/2 = 3.3% and they round it to 3%. Wtf (kine, 2018).​

D = Reference weight for a specific age group and gender

"The reference weights for adult women and men are 61 and 76 kg, respectively (see Chapter 1 [No (Wagner, 2018).])."​

E = Ratio of total body:liver vitamin A reserves

"The ratio of total body:liver vitamin A reserves is 10:9 (1.1) and is based on individuals with adequate vitamin A status."

Since the calculation is based on liver (which concentrates about 90% of the body poison), they's adding the remaining 10% to obtain the total body stores.

Liver stores = Body stores * 90/100
Liver stores = Body stores * 9/10
Liver stores * 10/9 = Body stores​

It's rounded to 1.1 for convenience.​

F = Efficiency of storage of ingested vitamin A

"Finally, the efficiency of storage can be determined by isotope dilution methods following the administration of either radioactive or stable-isotopically labeled vitamin A to subjects adequate in vitamin A (Bausch and Reitz, 1977; Haskell et al., 1997). Recent studies by Haskell and coworkers (1997) suggest that the efficiency of storage is approximately 40 percent, rather than the 50 percent that was previously reported (Olson, 1987)."

As they pointed out, adsorption of preformed poison is relatively constant in relation to propoison.

Efficiency of storage can be tricky because if you have low reserves, a greater portion tends to be utilized before it has a chance to be deposited, so it's lower. In the experiment it was about 30% compared to those with adequate reserves, which stored something close to 40% of the dose. So the more poisoned you is, the more you tend to accumulate it rather than use it right away.

GeForce driver is ready to be downloaded. Ok.

Therefore an estimated requirement without this factor will be suggesting (in theory) only about 40/100 of the need amount. Since the factor is known, they group it with the other factors on one side of the equation:

A × B × C × D × E = EAR * 40/100
A × B × C × D × E = EAR * 1/2.5
A × B × C × D × E × 2.5 = EAR

EAR: Estimated Average Requirement​

"By using this approach, a daily vitamin A intake can be determined that will assure vitamin A reserves to cover increased needs during periods of stress and low vitamin A intake. That value can be used for estimating the average requirement for vitamin A.

Based on these current estimations, the EAR of preformed vitamin A required to assure an adequate body reserve in an adult man is:

0.005 × {[20 μg/g × (0.03 × 76 kg)] × 1.1} × 2.5 = 627 μg RAE/day.
With a reference weight of 61 kg for women, the EAR would be 503 μg RAE/day."

(Liver weight)
[Total poison in liver]
{Total poison in the entire body} multiplied by the rate of depletion to know how much is lost a day so that you ingest at least this to maintain the burden and prevent a depletion, and the corrective factor for inefficiency. It's the essence of the current RDA.​

The 'Estimated Average Requirements' of 627 and 503 mcg of 'Retinol Activity Equivalents' for pimps and pimpesses now goes through more adjustments to cover those that use up the reserves faster (at the expense of those that doesn't), this goes back to the issues discussed in factor A (above).

"Based on the study of Sauberlich and coworkers (1974), Olson (1987) estimated that the liver vitamin A concentration was less than 10 μg/g at the time the first clinical signs of vitamin A deficiency appeared. From this assumption, it was estimated that the half-life of vitamin A is approximately 128 days, and the CV is 21 percent. Because the portion of this variability that is due to experimental error is not known, a CV of 20 percent is used for setting the RDA."

"The RDA for vitamin A is set by using a CV of 20 percent (see Chapter 1) using the EAR for adequate body stores of vitamin A. The RDA is defined as equal to the EAR plus twice the CV to cover the needs of 97 to 98 percent of the individuals in the group (therefore, for vitamin A the RDA is 140 percent of the EAR). The calculated values for the RDAs have been rounded to the nearest 100 μg."

View attachment 12332​

To cover the need of those that need more, you have to recommend more for those that needed less, whose requirements will be inflated. But it's challenging to provide generalized recommendations for a population.

- 627 mcg RAE * 140% = 878 mcg → 900 mcg RAE (3000 IU)/day for men
- 503 mcg RAE * 140% = 704 mcg → 700 mcg RAE (2300 IU)/day for women​

Pretty interesting. Main thing I took from that is that it can take 2+ years for some people to become depleted. This would explain cases like Grant. Grant also ate red beans for awhile, which he did not know had beta carotene in them. You could assume that he received enough A to keep him from the depletion state.

I understand your position more. You have read studies like this and so you think hey we have done this before, we have depleted vitamin A before, this is not some new thing, and it leads to bad things.

It's hard to make sense of that phenomena for something that's supposed to be absolutely essential. There's still so many unknowns...
How is Grant not breaking down after 4.5 years?
I was pleased to see @Amazoniac's posts about estimated time for depletion earlier in the thread.

I found this interesting as well. Are there other nutrients that once depleted become harder to absorb?

 

[Amazoniac]

Do you have access to the way they prepared the casein and tested it for for all types vitamin A?

It says that diet II has 23ug retinol per day, was the soy flour oxidized, again introducing retinoic acid(accutane)?

Soy beans per 100g
Vitamin A 180.00 IU 4 %
Vitamin A, RAE 9.00 mcg

No, but I'm not aware of soy having similar (binding) properties, so if that indeed occurred I suppose that casein would have haded a stronger sparing effect on bloody poison/"vitamin" A than soy, and it didn't happen. And if retinoic acid was present in considerable amounts, it could also have performed various rôles in place of the reserves, leaving more of the stored poison for vision and delay the appearance of problems for example.

And in terms of defattening, (especially in the case of soy) it makes no sense to damage its fats first through sterilization to only later extract them. If there's any residue, it must be quite small (oxidized or not). A soy product used in one of their previous experiments was named Bontrae by General Mills in case you want to search for it.

Not that it's safe to do it, but the issue appears exaggerated, you can ingest an entire tube of tretinoin cream (those for skin) without being toxic, a dose of 12500-25000 mcg of all-trannies retinoic acid.

 

[Blossom]

Are there other nutrients that once depleted become harder to absorb?

I’d like to find the answer to this question. At first glance it would seem the body is rejecting replenishing VA. Certainly their are things that aren’t optimal in our design like the fact that we don’t produce our own Vitamin C and the proximity of the airway and esophagus which makes us more prone to aspiration. The difficulty replenishing VA could be a flaw but then again maybe not. If anyone knows of other nutrients that the body treats similarly I’d be interested in knowing about them.

 

[sunraiser]

Pretty interesting. Main thing I took from that is that it can take 2+ years for some people to become depleted. This would explain cases like Grant. Grant also ate red beans for awhile, which he did not know had beta carotene in them. You could assume that he received enough A to keep him from the depletion state.

I understand your position more. You have read studies like this and so you think hey we have done this before, we have depleted vitamin A before, this is not some new thing, and it leads to bad things.



I found this interesting as well. Are there other nutrients that once depleted become harder to absorb?

Magnesium seems to have this profile. I found this when using iodine in mg doses and have seen others have the same issue. (completely depleting magnesium stores)

Seems to use up all your b6 and inhibit liver detox so replenishment seems to take both.

Vitamin A has interactions with magnesium and I wonder if it's not a big part of people's problems (large scale mag depletion).

 

[Makrosky]

Magnesium seems to have this profile. I found this when using iodine in mg doses and have seen others have the same issue. (completely depleting magnesium stores)

That's why the "iodine protocol" is for ? It includes magnesium.

And iodine will deplete everything just like any prometabolic substance will deplete everything. You run faster, you need more gas.

 

[InChristAlone]

Magnesium seems to have this profile. I found this when using iodine in mg doses and have seen others have the same issue. (completely depleting magnesium stores)

Seems to use up all your b6 and inhibit liver detox so replenishment seems to take both.

Vitamin A has interactions with magnesium and I wonder if it's not a big part of people's problems (large scale mag depletion).

If it was magnesium all of Dr. Smith's clients would have gotten better as he was big on supplementing mag. But they weren't.

 

[Amazoniac]

If it was magnesium all of Dr. Smith's clients would have gotten better as he was big on supplementing mag. But they weren't.

Do you know if he encourages most of his clients to use magnesium chloride? Because if so, it can lead to some nasty distortions with chronic use. I have suspected ever since he manifested a.. peculiar interest in this topic that it's being one of his personal motivations.

- Excess Magnesium Chloride Intake Causes Frank Acidosis

It's possible that Raj felt its effects before (perhaps it was not just a matter of contaminants):

- Ray Peat Email Exchanges - Ray Peat Forum Wiki

"In my own migraine experience, I found that a very small amount of either vitamin A or magnesium chloride could cause big headaches for two or three days. If I had put vitamin A anywhere on my face or arms, enough would touch my lips to cause the headache. It wasn't the vitamin A or magnesium itself that did it, but some very powerful allergen in the chemically manufactured products."​

 

[InChristAlone]

Do you know if he encourages most of his clients to use magnesium chloride? Because if so, it can lead to some nasty distortions with chronic use. I have suspected ever since he manifested a.. peculiar interest in this topic that it's being one of his personal motivations.

- Excess Magnesium Chloride Intake Causes Frank Acidosis

It's possible that Raj felt its effects before (perhaps it was not just a matter of contaminants):

- Ray Peat Email Exchanges - Ray Peat Forum Wiki

"In my own migraine experience, I found that a very small amount of either vitamin A or magnesium chloride could cause big headaches for two or three days. If I had put vitamin A anywhere on my face or arms, enough would touch my lips to cause the headache. It wasn't the vitamin A or magnesium itself that did it, but some very powerful allergen in the chemically manufactured products."​

Why would he chalk that up to an allergen? Headaches are a sign of vitamin A toxicity. I rarely get a headache even with all my "contaminated" ascorbic acid use. About the only time I ever get a headache is if I'm in caffeine withdrawal or have a reactive hypoglycemic response to a large protein meal.

Yes Smith is big on mag chloride. But he has also used other oral forms with his clients.

 

[Amazoniac]

Why would he chalk that up to an allergen? Headaches are a sign of vitamin A toxicity. I rarely get a headache even with all my "contaminated" ascorbic acid use. About the only time I ever get a headache is if I'm in caffeine withdrawal or have a reactive hypoglycemic response to a large protein meal.

Yes Smith is big on mag chloride. But he has also used other oral forms with his clients.

I also think that it was a sign of taking too much or not handling it well:
- Grant Genereux's Theory Of Vitamin A Toxicity

Orion and other gurus have used retinoic acid and accutane interhealcheaghsbly but it can be misleading; it depends on the form (there's tretinoin, isotretinoin, alitretinoin), just like the analogs of calcitriol.

 

[sunraiser]

That's why the "iodine protocol" is for ? It includes magnesium.

I personally took magnesium - it only made me worse without B6.

If it was magnesium all of Dr. Smith's clients would have gotten better as he was big on supplementing mag. But they weren't.

I didn't mean it's just magnesium, only that being depleted can give quite specific needs to get "undepleted". I eat 400mg magnesium a day and have sometimes needed 400-600mg on top. Whether that's because of inflammation via poor liver detox phases or lymph stagnation or lots of unknown factors I don't know.

Vitamin A as retinol is demanding resources that may not be available including copper and zinc, but magnesium is intricately woven into allowing zinc and copper to be repleted (as is calcium, if only indirectly). It can be a core factor in repletion of many of the things vitamin A "asks for". I think a big one is liver detox as if you can't resolve this then you won't have the digestion and appetite to uptake the calories you need to recover from the metabolic demands from high vit A intake.

When magnesium is severely deficient then B6 is used up to help [push magnesium into the cells?], and for me that has involved cravings not being enough to restore levels (just a few mg, though). I also have problems with chloride, though it has worked for me in the very short term in the past.

Then there are the trace minerals which are going to be a problem when people are only eating refined starches and fruit. My point was that magnesium depletion, when enforced by non-intuitive or non physiological means, seems to need some intervention to recover from.

These are more personal reflections though, as the stuff about eyelid discolouration and excema (spelling?) are not ones I've encountered despite accutane usage and lots of liver eating.

I'd be interested in seeing the exact symptoms people are seeing very noticable improvements in from the pool of people that are doing well in this elimination diet. People have mentioned various bits and bobs but it'd be good to compile or create a concise list.