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

[Amazoniac]

- The metabolic availability of vitamin A (Retinol) in streptozotocin-induced diabetic rats

Spoiler

They gaved zinc thinking that it could normalize trafficking (binding proteins).

 

[Amazoniac]

- Retinol oxidation to retinoic acid in human thyroid glandular cells

Spoiler

"It is now recognized that retinoid binding proteins participate in RA biosynthesis and there is compelling evidence that retinoids bound to cellular retinoid binding proteins (CRBPs) are better substrates for the enzyme catalysis with respect to free, unbound retinoids[19,20]. In particular, Ottonello et al.[20] revealed the presence of a cytosolic enzyme system in calf liver that uses CRBP-bound retinol for its direct oxidation to retinoic acid. The role of XDH in the retinoic acid biosynthesis and the implication of CRBP(s) in this process have been described by us in epithelial tissues characterized by a functional dynamism as the breast tissue[19]. The under expression of CRBP(s)[21–23] and/or XDH[23] in human breast cancer has been considered to be responsible for RA-deficient biosynthesis."

"It is well known that xanthine oxidoreductase (XOR), the complex enzyme system that catalyzes the two terminal steps in purine catabolism, exists in two interconvertible forms: XDH and XO. A substantial distinction between XDH and XO is that XDH, the physiological form of the enzyme in cells, reduces NAD+ without superoxide generation, whereas XO, the modified form, uses molecular oxygen as electron acceptor and generates superoxide anion as a product. Conversion of XDH into XO can occur through oxidation of sulfhydryl residues of cysteine that decreases NAD+ dependence or as a consequence of limited proteolysis[30]."

- Advanced Nutrition and Human Metabolism (978-1-133-10405-6)

Reposting for convenience:
- Retinal dehydrogenase - Wikipedia
- Retinal oxidase - Wikipedia​

"XDH activity is subject to both transcriptional and translational control by mechanisms that are modulated by hormones (including oestrogen and/or angiotensin II), cytokines and oxygen tension, eventually leading to its transition to the oxidase form, which moves outside the cell[37,38]." ??

"The study by Cheung et al.[32] on the characterization of XOR as a novel regulator of adipogenesis in 3T3-L1 cells is extremely interesting. XOR lies in fact downstream of C/EBPb and upstream of PPAR-g, in the cascade of factors that control adipogenesis. The authors demonstrate that XOR expression and activity are closely regulated, with a robust increase during the first 24 h after initiation of differentiation and a return to basal levels within day 3. The authors also suggest that XOR produces an extractable component that has the ability to activate PPAR-g. In addition, other reports indicate that the adipogenic activity of the xor gene may be mediated by the XDH activity of XOR[32]. These observations have prompted us to hypothesize that the extractable component[33] produced by XDH is retinoic acid, this latter being responsible for the effects on adipogenesis and activity of PPAR-g[39–40]. There is some evidence that atRA can be proadipogenic or antiadipogenic in vivo, depending on the dose. atRA is in fact a powerful inhibitor when used at relatively high doses (0.1–10 mM) in early stages of adipogenesis[41], whereas it promotes adipogenesis at lower doses (1 pM to 10 nM range)[42]."

"Multiple evidences also support a link between thyroid gland and retinoids. Several studies have reported that both a deficiency or an excess of vitamin A affect thyroid gland volume acting on the thyroid stimulating hormone synthesis and that high vitamin A doses result in a decline of serum levels of T3 and T4 in the rat[46,47]."

"The suggestion by Xu et al.[48] that XDH plays a role in human development is consistent with the present evidence that this enzyme also presides over retinoic acid biosynthesis in thyroid glandular cells. Our results demonstrate that in these cells, which do not express any retinol dehydrogenase, XDH, supported by CRBPs, directly oxidizes ROL to RA without release of RAL in the medium. Another finding in support of the equivalence between retinol dehydrogenase and XDH is the complete loss of catalytic activity, toward atROL and xanthine, of the purified enzyme fraction that we observe after treatment with anti-bovine XO/AO antibodies."

"[..]the non-release of RAL in the cytoplasm as intermediate substrate during retinol oxidation, preventing the competition with ROL for the binding to CRBP1, avoids the slow-down or the block of the biosynthetic pathway. Thus, we propose this enzyme as eligible for the direct oxidative catalysis of retinol bound to CRBP1 (holo-CRBP1) also in human thyroid glandular cells (see scheme in Figure 5)."

Not depending on NAD is cool. Yet, morbydenum and glourine are still needed. Their shortage should also affect sulfur metabolism (poisonal and sulfite oxidase), something that can be made worse with the lack of nutrients that are easily lost in chronic inflammation, such as zinc and pyridoxine.

- Metabolism of Dietary and Microbial Vitamin B Family in the Regulation of Host Immunity

"Vitamin B6 deficiency disrupts the Th1–Th2 balance toward an excessive Th2 response, resulting in allergy (85). Moreover, low plasma vitamin B6 levels, together with increased levels of pro-inflammatory cytokines such as TNF-α and IL-6, have been observed in patients with rheumatoid arthritis (86)."​

Messing up sulfur metabolism might disturb poisonoids handling because various proteins require it at the interacting sites, sometimes these aren't apparent because they work on intermediate metabolites.

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- Vitamin A aldehyde-taurine adduct and the visual cycle

Spoiler

"Although retinaldehyde molecules are critical to vision, they are also hydrophobic and highly reactive. To facilitate the movement of retinoids through the visual cycle and to prevent nonspecific chemical reaction the visual cycle utilizes multiple mechanisms for handling these molecules when they are not sequestered within the binding pockets of opsin (1). For example, multiple species of dehydrogenases are available to reduce retinaldehydes; these enzymes, by converting the aldehyde to an alcohol, limit the quantities of retinaldehyde (2, 3). Additionally, the aqueous soluble carrier cellular retinaldehyde-binding protein (CRALBP) in RPE and Müller cells chaperones 11cisRAL, thereby reducing product inhibition of the isomerase activity, maintaining the cis-isomer state of 11-cis-retinal and protecting against the reactivity of the aldehyde (4–8)."

"All-trans-retinal released from photoactivated opsin can be picked up by neighboring phosphatidylethanolamine (PE) in the disk membrane, thereby forming the reversible Schiff base, N-retinylidene-PE (NRPE) (9–11), that sequesters the reactive aldehyde and may enable nonenzymatic visual pigment renewal (11, 12). NRPE is also recognized as the ligand that binds the photoreceptor-specific ATP-binding cassette transporter (ABCA4) in outer segments (13–19). The function of ABCA4 is to transport nonprotonated NRPE across the lipid bilayer from the interior of the disk to the cytoplasmic face of the disk membrane, where all-trans-retinaldehyde (atRAL) is released and subsequently reduced to the less reactive alcohol (all-trans-retinol) by NADPH-dependent retinol dehydrogenases (RDH8, RDH11, and RDH12) (2, 18, 20–23). The 11-cis isomer of NRPE (N-11-cis-retinylidene-PE) can also be transported by ABCA4 from the inner disk to the cytoplasmic leaflet of disk membranes; this is a role that is presumed to prevent excess levels of 11-cis-retinal (17, 20)."

Inefficient removal of the NRPE isomers is a hazard since this Schiff base conjugate can react with a second molecule of all-trans-retinal instead of hydrolyzing to PE and all-trans-retinal. This second irreversible condensation reaction is the first step in a nonenzymatic synthetic pathway leading to the formation of fluorescent di-retinal compounds within the lipid bilayers of the photoreceptor outer segment. These compounds include the phosphatidyl-pyridinium bisretinoid, A2PE; the pyridinium bisretinoids A2E and A2-GPE; the phosphatidyl-dihydropyridine bisretinoid, A2-DHP-PE; and both all-trans-retinal dimer and the related PE conjugate, all-trans-retinal dimer-PE (20, 24). Phagocytosis of shed outer segments by RPE results in the accumulation of these toxic compounds in RPE cells.

It was recognized a number of years ago that retinaldehyde also combines with the endogenous sulfur-containing amino acid taurine to produce the taurine-retinaldehyde Schiff base, A1-taurine (A1T) (25) (Fig. 1). Taurine contains a sulfonic acid group in place of the typical carboxylic group of an amino acid and it carries a primary amine. Taurine is not incorporated into protein but in a study of 110 metabolites representative of all major metabolic pathways, only uptake of proline by RPE was greater than taurine (26). Although taurine is abundant in neural retina, its function is poorly understood and little or no attention is paid to A1T."

"There are other differences between NRPE and A1T. For example, NRPE bears hydrophobic long-chain fatty acids and is expected to exist in a hydrophobic environment. On the other hand, A1T is an amphiphilic small molecule carrying a negatively charged sulfonated group together with a hydrophobic retinoid moiety (Fig. 1); as such, A1T may represent a mechanism in photoreceptor cells for escorting retinaldehyde, a molecule that is otherwise poorly soluble in an aqueous milieu. As noted above, NRPE is the ligand that is recognized by ABCA4 in its effort to remove reactive retinaldehyde from photoreceptors after photon absorption. NRPE has also been suggested to function in the photoregeneration of visual pigment by light-dependent conversion of all-trans-NRPE to its 11-cis isomer (46)."

Formation of a di-retinal is worse than 4 minutes without air, 4 days without water, 4 months without food, a meteor striking the earth or getting vaccinated. Reminded me of death dialdehydes [as in malonicdialdehyde] that can appear from non-central cleavage of macabrotenes, but in this case the same molecule is cleaved twice, leaving the core with an aldehyde group on each side (plant research).

Spoiler

You can probably find relationships between alcoholic compounds with poisonol (cholesterol, ethanolamine, choline, inositol, serine). Some of them are metabolized similarly: pyridoxine/pyridoxol → pyridoxal → pyridoxic acid, choline → betainaldehyde → betaine.
- Alcohol oxidation by flavoenzymes

I was reading one article that had a typo: all-trance instead of all-trans. Prolactinese has now a new term.

 

[tim333]

Asking this question as I kept my retinol intake around 290 iu a day for a couple of months while supplementing vitamin d and eating fish/some avocado daily. by the end of this period my sebum production was completely recovered back to how it was as a teenager. I developed extreme dry skin last January after overdosing on liver. Skin seems less prone to infection with all the oil however it’s a bit too much so I took a multi with 600 iu retinol acetate three days in a row. Oil on my cheeks has been reduced already and I feel significantly warmer even though temps are not much higher. Problem is I got a headache very soon after the first dose, vision became less focused, very strong fatigue happening, an almost constant low grade headache and a very tense jawline.

could all this be happening from this small dose (1800 iu) and is it caused by something that has been depleted?

I think the chance that you have low vA levels after a couple of months is very low. One of the symptoms of Hypervitaminosis A is excess sebum. Paradoxically people with Hypervitaminosis A often have symptoms improve when consuming more vA. Something to do with release of stored vA causes more symptoms it seems. When I was consuming a lot of vA it never reduced my excess sebum. Low vA hasn't changed it noticeably, it certainly hasn't got worse.

 

[tim333]

Improvements came slowly (no honeymoon period for me) after 6 months and are now, after 18 months, really noticable: markedly less fatigued, a lot less anxiety, more mental focus, better sleep, emotionally more stable, less OCD/autistic behaviour. Serum retinol has dropped from 40 to 18 mcg/dL. The only thing that has barely improved is my inflamed gut and associated food intolerances. As long as I stick to this insanely strict diet, I'm doing really well but once I start deviating too much (while experimenting), the gut starts acting up and my energy level quickly follows.

I can't see how you will benefit from a low vA diet now that your serum retinol is 18 mcg/dL.

 

[Amazoniac]

- Metabolism, Plasma Transport and Biliary Excretion of Radioactive Vitamin A and Its Metabolites as a Function of Liver Reserves of Vitamin A in the Rat

Spoiler

"Administered retinol and retinoic acid are converted in the liver to oxidized and/or conjugated metabolites that are rapidly excreted in the bile (7, 17-20). When liver stores of vitamin A are prelabeled with radioactive vitamin A, the rate of biliary excretion of labeled metabolites of vitamin A is fairly constant (21). In our present studies, we show that the rate of excretion of vitamin A metabolites is independent of liver stores of vitamin A up to about 30 mcg/g, but then increases rapidly to plateau at an eight times greater rate at a liver vitamin A concentration of 140 mcg/g. In essence, an oxidative and/or conjugative mechanism is induced at a specific intake or liver reserve of vitamin A that results in a close proportionality between biliary excretion of vitamin A metabolites and liver reserves between 30 and 140 mcg/g liver, a range characteristic of the liver stores of well-nourished humans and experimental animals (21). In this regard, the 4-hydroxylation of retinoic acid in the liver is known to be induced by high intakes of the substrate (22)."

"Our observations on the inducible system acting on vitamin A in the liver clarify past observations on the relationship between liver stores and the rate of vitamin A excretion. When liver reserves of vitamin A are ample, their rate of depletion on a vitamin A-free diet is a first-order process (23). When liver stores are low, on the other hand, the depletion rate is much slower (23). Similarly, Varma and Beaton (16) found that the excretion of radioactive vitamin A metabolites in the feces and urine 8 days after the administration of a radioactive dose of vitamin A to older rats was independent of the liver vitamin A concentration up to approximately 60 mcg/g and only increased markedly at values greater than 120 mcg/g. Although the qualitative response was the same, the induction process occurred in their studies at a much higher liver vitamin A concentration than in ours. Possible reasons for these differences in threshold are: 1) that bile excretion is a more sensitive indicator of the induced process than fecal excretion, particularly when the modulating effects of the enterohepatic circulation are considered, 2) that our rats were significantly younger than theirs and 3) that our rats were maintained on a specific dosage schedule of vitamin A through the experiment, whereas theirs were placed on a vitamin A-deficient diet for 8-10 weeks, were fed graded doses of vitamin A for 4 days and then were treated with radioactive vitamin A."

"Varma and Beaton (16) suggested that the basal rate of vitamin A metabolism at low liver stores was 4.4 mcg retinol/day, of which excretion in the urine and feces accounted for 3.0 and 1.4 mcg/day, respectively. If we assume a daily bile flow of 10 ml in a 200-g rat (21) and a recovery from the enterohepatic circulation of 30%, the mean fecal excretion of metabolites at low liver reserves in our study would be 0.28 mcg/ml x 10 ml x 0.7, or 2.0 mcg/day. Although urinary excretion of metabolites predominated in the study of Varma and Beaton (16), others have found that the fecal excretion of vitamin A metabolites exceeds that in the urine (24). In either case, the basal excretion rates are similar and in accord with our observation, as well as that of others (23), that a daily dose of 5 mcg retinol/day gave essentially no storage in young rats."

"Our present studies have implications relative both to the assessment of vitamin A status and to the daily allowance of the vitamin. Inasmuch as the turnover of vitamin A is roughly a first-order process at intermediate (30-140 mcg/g) concentrations of vitamin A in the liver, the hope has persisted that measurement of specific metabolites of vitamin A in the urine or feces might yield information about marginal or poor vitamin A status. Unfortunately, this hope will probably not be realized, largely because the total excretion of vitamin A metabolites in the critical range of liver reserves (0-30 mcg/g) is independent of liver stores."

"The recommended daily allowance of a nutrient is often selected on the basis of balance studies and the expected or measured variance in a population. Similar information might also be gained by observing metabolic changes that occur as the daily dose of a nutrient increases. With vitamin A, two such changes occur in rats: 1) as the liver reserves increase from very low values, the steady-state plasma vitamin A concentration approaches a plateau value at a liver concentration of 5-10 mcg/g, both in our study and in that of Varma and Beaton (16) and 2) as liver reserves and intakes increase further, the rapid biliary excretion of vitamin A metabolites is induced rather sharply at a liver level just over 30 mcg/g. Thus, a liver vitamin A concentration of 20 mcg/g might ensure saturation of the plasma vitamin A transport system and yet not induce the special excretory pathway. Although similar data on humans are needed to validate any specific recommendation in this regard, a vitamin A concentration of 20 mcg retinol per gram of liver has been suggested on other grounds as a minimally adequate reserve in both children and adults (25, 26)."

- The Vitamins: Fundamental Aspects in Nutrition and Health (978-0-12-802965-7)

Spoiler

 

[tim333]

@Amazoniac Figure 6.5 is a nice chart but is misleading because the normal range varies by age. People in their twenties have a lower normal serum retinol level than that.

 

[Belsazar]

Stumbled upon this case study. Look at Figure 2 and Figure 3.

​

Refractory hypercalcemia owing to vitamin A toxicity in a 4-year-old boy (DOI: Refractory hypercalcemia owing to vitamin A toxicity in a 4-year-old boy)​

Initial investigations were significant for severe hypercalcemia, hyponatremia, hypokalemia, mildly elevated creatinine, elevated C-reactive protein, leukocytosis and normocytic anemia

The patient’s main sources of vitamin A included 1–2 cups of kale, 2–3 cups of green vegetables, 2–3 cups of fruit and 4 oz of meat per day (nonliver), plus a multivitamin containing vitamin A as β-carotene (28 μg RAE). He had previously been taking cod liver oil supplements (276 μg/day RAE) for more than 1 year, but had stopped many months previously.

Vitamin A toxicity is an important diagnosis to consider in patients with hypercalcemia. Although our patient had classic findings of vitamin A toxicity, his case had unique features that made the diagnosis challenging, including toxic ingestion with predominantly provitamin A rather than preformed vitamin A, refractory hypercalcemia and bicytopenia despite a normal bone marrow biopsy. Chronic vitamin A toxicity is particularly challenging, as toxicity may occur at what people perceive as a “safe doses” of vitamin A from dietary sources and supplementation.

Based on this, does anyone know more about Vitamin A and/or hypercalcemia and its connection to hyponatremia/hypokalemia?

 

[Belsazar]

Finally measured my Vitamin A too, Came back at the top of the range after 2 months of low Vitamin A diet. Dont know what to take of it, since the liver will recruit it most probably from storage and on top of it my Vit D is low. But I do have a history of Vitamin A supplementation, high intake from diet and retinoid treatments.

Do you guys know if Vitamin A "elimination" can temporarily cause elevated liver enzymes? Any experiences from your blood tests?

 

[Vinero]

I posted 2 years ago that during the healthiest period of my life I was unintentionally eating a low vitamin A diet consisting of beef, chicken, white rice, potatoes, low fat milk, and dark chocolate.
However, one important part I left out/forgot was that I always cooked everything in butter. Meat was fried in butter. Potatoes were fried in butter. When eating bread or rice I added some butter to make it palatable.
I was probably eating around 30 gram of butter per meal. 30 gr of butter x 3 meals a day = close to 100 gr of butter a day.
100 gr of butter has 2500 IU of vitamin A. I also drank around 1-2 quarts of non-fortified low fat milk a day. I was probably getting around 3000 IU a day total. That's pretty much the RDA is it not?
It seems that the diet I was eating during the healthiest period of my life wasn't low vitamin A at all. It contained a normal amount of vitamin A as retinol, but it was low in carotenoids.
So.. Maybe the good health I experienced when eating that diet had nothing to do with being low vitamin A.
Maybe it was just a good diet: low PUFA, high saturated fat, high carb, adequate protein, and low in things that block thyroid function like carotene, goitrogens, excessive fluid consumption etc.

This is in line with what Ray Peat says. That retinol is good and essential, but that carotene blocks thyroid function.
"I avoid carotene, because it blocks thyroid and steroid production, and very large, excessive, amounts of vitamin A, retinol, can do the same.”

“If your cholesterol is above 200, and the thyroid supplements didn’t warm you up, it’s possible that something is interfering with your steroid synthesis, which might be a deficiency of something like vitamin A, or interference from something like iron or carotene.”

 

[LLight]

@Vinero

Did you start drinking coffee between both experiences?

Spoiler

I stay on my impression, in some people, coffee seems to have a really bad effect (that may stem from a disturbance of vitamin A metabolism). It's clearly not the 'liver cleansing' story for everybody. Some people have post-acute withdrawal symptoms for months, slowly regaining their energy, improving their anxiety and digestion.

 

[Vinero]

@Vinero

Did you start drinking coffee between both experiences?

Spoiler

I stay on my impression, in some people, coffee seems to have a really bad effect (that may stem from a disturbance of vitamin A metabolism). It's clearly not the 'liver cleansing' story for everybody. Some people have post-acute withdrawal symptoms for months, slowly regaining their energy, improving their anxiety and digestion.

No, I have always drank coffee. I have drank coffee when in great health as well as when in I was in poor health suffering from eczema and asthma.

I remember my health began to decline when I started "strictly peating" eating lots of cheap low fat cheese, and drinking lots of orange juice. But the cheap low fat cheeses that I was relying on as my main source of protein had added beta carotene or annatto as coloring agents. So I was getting a lot of carotenoids without being aware of it. The health problems that I developed when I was peating could have been the result of high carotenoid intake. Not because I had too much retinol. There is a study on how supplemental beta carotene increases risk of lung cancer. I was having severe lung problems during peating (asthma and frequent lung infections)

If I was going to eat cheese nowadays I would buy quality cheeses, like Swiss, Italian and French cheese containing animal rennet and no coloring agents. Examples of high quality cheeses are parmiggiano reggiano, emmentaler, gruyere, comté, beaufort, pecorino romano and more. I would just make sure it has no added beta carotene or annatto.

 

[Korven]

I posted 2 years ago that during the healthiest period of my life I was unintentionally eating a low vitamin A diet consisting of beef, chicken, white rice, potatoes, low fat milk, and dark chocolate.
However, one important part I left out/forgot was that I always cooked everything in butter. Meat was fried in butter. Potatoes were fried in butter. When eating bread or rice I added some butter to make it palatable.
I was probably eating around 30 gr of butter per meal. 30 gram of butter x 3 meals a day = close to 100 gram or butter a day.
100 grams of butter has 2500 IU of vitamin A. I also drank around 1-2 quarts of low fat milk a day. I was probably getting around 3000 IU a day total. That's pretty much the RDA is it not?
Conclusion: The diet I was eating during the healthiest period of my life contained a normal amount of vitamin A as retinol, but it was low in carotenoids.
So.. Maybe the good health I experienced when eating that diet had nothing to do with being low vitamin A.
Maybe it was just a good diet: low PUFA, high saturated fat, high carb, adequate protein, and low in things that block thyroid function like carotene, goitrogens, excessive fluid consumption etc.

This is in line to what Ray Peat says. That retinol is good and essential, but that carotene block thyroid function.
"I avoid carotene, because it blocks thyroid and steroid production, and very large, excessive, amounts of vitamin A, retinol, can do the same.”

100% this.

The best I've felt and looked was on a diet of beef, chicken, white rice, pasta, bread, and lots of butter and milk. No fruits and vegetables because I didn't enjoy eating them. Felt very androgenic, glowing skin, good sleep, good digestion etc. Then I went vegan, loaded up on millions IU of beta carotene/oxalates/antinutrients and basically destroyed my body and digestive tract.

On a low VA diet of mostly beef, rice, beans it felt like my body stopped hormone production, like I was on a vegan diet again. Skin barrier function got progressively worse, probably due to insufficient steroid production. Mood swings and depression. On Grant Genereux's forum there are several people basically falling apart eating low VA. Especially younger people seems like, higher requirements for retinol or less stored in liver and body fat?

Now I've come full circle and am back to eating my previous bodybuilding diet + supplementing 1 grain thyroid. Seems to be working pretty well, I feel warm and happy.

I think other potential issues with high VA fruits and vegetables besides carotenoids are salicylates, oxalates and fructose. OJ and aspirin guaranteed to make ezcema flare up for me. Liver is sketchy and I don't see myself eating it again.

 

[gaze]

100% this.

The best I've felt and looked was on a diet of beef, chicken, white rice, pasta, bread, and lots of butter and milk. No fruits and vegetables because I didn't enjoy eating them. Felt very androgenic, glowing skin, good sleep, good digestion etc. Then I went vegan, loaded up on millions IU of beta carotene/oxalates/antinutrients and basically destroyed my body and digestive tract.

On a low VA diet of mostly beef, rice, beans it felt like my body stopped hormone production, like I was on a vegan diet again. Skin barrier function got progressively worse, probably due to insufficient steroid production. Mood swings and depression. On Grant Genereux's forum there are several people basically falling apart eating low VA. Especially younger people seems like, higher requirements for retinol or less stored in liver and body fat?

Now I've come full circle and am back to eating my previous bodybuilding diet + supplementing 1 grain thyroid. Seems to be working pretty well, I feel warm and happy.

I think other potential issues with high VA fruits and vegetables besides carotenoids are salicylates, oxalates and fructose. OJ and aspirin guaranteed to make ezcema flare up for me. Liver is sketchy and I don't see myself eating it again.

i think this is why the starch+ meat is needed for so many people. the insulin kick from starch is the most anabolic hormone we have, and because of that it strongly opposes adrenaline and cortisol which allows the liver to start storing glycogen. i suspect insulin is also required in T3 production to a certain degree , which is why carbs from starch feels more long lasting than sugar for a lot of people. when you can store glycogen, then all of the peaty foods start working. that's why i think OJ and milk are good additions to a diet cause they boost metabolic function, but using those two foods as the main staples of the diet tends to always go wrong.

 

[ursidae]

100% this.

The best I've felt and looked was on a diet of beef, chicken, white rice, pasta, bread, and lots of butter and milk. No fruits and vegetables because I didn't enjoy eating them. Felt very androgenic, glowing skin, good sleep, good digestion etc. Then I went vegan, loaded up on millions IU of beta carotene/oxalates/antinutrients and basically destroyed my body and digestive tract.

On a low VA diet of mostly beef, rice, beans it felt like my body stopped hormone production, like I was on a vegan diet again. Skin barrier function got progressively worse, probably due to insufficient steroid production. Mood swings and depression. On Grant Genereux's forum there are several people basically falling apart eating low VA. Especially younger people seems like, higher requirements for retinol or less stored in liver and body fat?

Now I've come full circle and am back to eating my previous bodybuilding diet + supplementing 1 grain thyroid. Seems to be working pretty well, I feel warm and happy.

I think other potential issues with high VA fruits and vegetables besides carotenoids are salicylates, oxalates and fructose. OJ and aspirin guaranteed to make ezcema flare up for me. Liver is sketchy and I don't see myself eating it again.

Why did you try to go vegan?

 

[Vinero]

100% this.

The best I've felt and looked was on a diet of beef, chicken, white rice, pasta, bread, and lots of butter and milk. No fruits and vegetables because I didn't enjoy eating them. Felt very androgenic, glowing skin, good sleep, good digestion etc. Then I went vegan, loaded up on millions IU of beta carotene/oxalates/antinutrients and basically destroyed my body and digestive tract.

On a low VA diet of mostly beef, rice, beans it felt like my body stopped hormone production, like I was on a vegan diet again. Skin barrier function got progressively worse, probably due to insufficient steroid production. Mood swings and depression. On Grant Genereux's forum there are several people basically falling apart eating low VA. Especially younger people seems like, higher requirements for retinol or less stored in liver and body fat?

Now I've come full circle and am back to eating my previous bodybuilding diet + supplementing 1 grain thyroid. Seems to be working pretty well, I feel warm and happy.

I think other potential issues with high VA fruits and vegetables besides carotenoids are salicylates, oxalates and fructose. OJ and aspirin guaranteed to make ezcema flare up for me. Liver is sketchy and I don't see myself eating it again.

Seems like a diet build on milk, meat and refined starch produced good results for us in the past. The moderate amounts of retinol/retinyl esters found in foods such as butter and milk don't cause any problems. We've both have had the experience of having awesome health when eating those foods. It's the leafy greens and brightly coloroed fruits that provide a lot of carotenoids that slow metabolism by interfering with thyroid function

This would explain why most people when they start the low vitamin A diet feel very good the first 6 months. They cut out all sources of vitamin A including carotenoids. The drop in carotenoids allows their thyroid to function again normally. Result: they feel amazing, thyroid function is close to 100% and they still have stored retinol/vitamin A in their liver to support steroid synthesis.

After a year or so the retinol/vitamin A concentrations in the liver begin to get very low. The following symptoms can occur which are then said to be vitamin A detox symptoms, but look very similar to symptoms of hypothyroidism or a low metabolic rate.

-Dry, itchy, red skin. Particularly around the face, ears, and neck.
-Acne on back, lots of bumps and pimples on body or face
-Low libido
-Depressed, no motivation.
-Random anxiety
-Feeling cold a lot
-Eye problems, like nightblindness, blurry vision, dry eyes, and seeing halos around lights (which could be a sign of cataracts)


What is a person to do when they are at this point? When they are clearly experiencing signs of a poorly functioning metabolism. Do they start eating real vitamin A again from sources like butter, cream, milk, or even a piece of liver?
Or do they continue to push on trying to deplete vitamin A with the expectation that great health will await them once they finally deplete their vitamin A stores? The latter approach is a dangerous one if it turns out that retinol is a vitamin after all, needed for healthy skin and vision. What if a person develops cataracts or other forms of eye-damage during the detox process?

 

[Vinero]

i think this is why the starch+ meat is needed for so many people. the insulin kick from starch is the most anabolic hormone we have, and because of that it strongly opposes adrenaline and cortisol which allows the liver to start storing glycogen. i suspect insulin is also required in T3 production to a certain degree , which is why carbs from starch feels more long lasting than sugar for a lot of people. when you can store glycogen, then all of the peaty foods start working. that's why i think OJ and milk are good additions to a diet cause they boost metabolic function, but using those two foods as the main staples of the diet tends to always go wrong.

I agree. I don't get that satisfied feeling after a meal if it didn't have starch like white rice or bread in it.

 

[Korven]

i think this is why the starch+ meat is needed for so many people. the insulin kick from starch is the most anabolic hormone we have, and because of that it strongly opposes adrenaline and cortisol which allows the liver to start storing glycogen. i suspect insulin is also required in T3 production to a certain degree , which is why carbs from starch feels more long lasting than sugar for a lot of people. when you can store glycogen, then all of the peaty foods start working. that's why i think OJ and milk are good additions to a diet cause they boost metabolic function, but using those two foods as the main staples of the diet tends to always go wrong.

Yeah I think starch can be pretty awesome if someone doesn't get weird inflammatory/endotoxin poisoning symptoms from it. In the past I have noticed certain symptoms getting better on a zero starch approach, but then after a few weeks I feel like I'm starving from a lack of glucose so it's not really sustainable. I think an individual have to experiment and determine whether starch is a net positive or negative.

Why did you try to go vegan?

Ethical reasons. Then I also became convinced a strict plant-based diet was the optimal diet for humans... Took 3 years for me to realize I was falling apart

Seems like a diet build on milk, meat and refined starch produced good results for us in the past. The moderate amounts of retinol/retinyl esters found in foods such as butter and milk don't cause any problems. We've both have had the experience of having awesome health when eating those foods. It's the leafy greens and brightly coloroed fruits that provide a lot of carotenoids that slow metabolism by interfering with thyroid function

This would explain why most people when they start the low vitamin A diet feel very good the first 6 months. They cut out all sources of vitamin A including carotenoids. The drop in carotenoids allows their thyroid to function again normally. Result: they feel amazing, thyroid function is close to 100% and they still have stored retinol/vitamin A in their liver to support steroid synthesis.

After a year or so the retinol/vitamin A concentrations in the liver begin to get very low. The following symptoms can occur which are then said to be vitamin A detox symptoms, but look very similar to symptoms of hypothyroidism or a low metabolic rate.

-Dry, itchy, red skin. Particularly around the face, ears, and neck.
-Acne on back, lots of bumps and pimples on body or face
-Low libido
-Depressed, no motivation.
-Random anxiety
-Feeling cold a lot
-Eye problems, like nightblindness, blurry vision, dry eyes, and seeing halos around lights (which could be a sign of cataracts)


What is a person to do when they are at this point? When they are clearly experiencing signs of a poorly functioning metabolism. Do they start eating real vitamin A again from sources like butter, cream, milk, or even a piece of liver?
Or do they continue to push on trying to deplete vitamin A with the expectation that great health will await them once they finally deplete their vitamin A stores? The latter approach is a dangerous one if it turns out that retinol is a vitamin after all, needed for healthy skin and vision. What if a person develops cataracts or other forms of eye-damage during the detox process?

Great summary - couldn't have said it better myself.

The only mystery that remains... why isn't Grant blind yet? Maybe his body has gone into hibernation mode, sparing the few retinol molecules left in his body for the rods in the retina? Unless everything we know about phototransduction is completely wrong Rhodopsin (which sounds unlikely).

 

[Deleted member 5487]

i think this is why the starch+ meat is needed for so many people. the insulin kick from starch is the most anabolic hormone we have, and because of that it strongly opposes adrenaline and cortisol which allows the liver to start storing glycogen. i suspect insulin is also required in T3 production to a certain degree , which is why carbs from starch feels more long lasting than sugar for a lot of people. when you can store glycogen, then all of the peaty foods start working. that's why i think OJ and milk are good additions to a diet cause they boost metabolic function, but using those two foods as the main staples of the diet tends to always go wrong.

Gelatinized Starch is a crucial component to any diet.

 

[Deleted member 5487]

Yeah I think starch can be pretty awesome if someone doesn't get weird inflammatory/endotoxin poisoning symptoms from it. In the past I have noticed certain symptoms getting better on a zero starch approach, but then after a few weeks I feel like I'm starving from a lack of glucose so it's not really sustainable. I think an individual have to experiment and determine whether starch is a net positive or negative.



Ethical reasons. Then I also became convinced a strict plant-based diet was the optimal diet for humans... Took 3 years for me to realize I was falling apart



Great summary - couldn't have said it better myself.

The only mystery that remains... why isn't Grant blind yet? Maybe his body has gone into hibernation mode, sparing the few retinol molecules left in his body for the rods in the retina? Unless everything we know about phototransduction is completely wrong Rhodopsin (which sounds unlikely).

Most inflammatory cytokines and endotoxin come from excess fat.

 

[mrchibbs]

What is a person to do when they are at this point? When they are clearly experiencing signs of a poorly functioning metabolism. Do they start eating real vitamin A again from sources like butter, cream, milk, or even a piece of liver?

I think this is where the insights we've learned about vitamin A in the past 2 years are important. Ray was saying those things before, and it was in textbooks in the 30s-40s but I don't think it was emphasized anough.

When people are experiencing those symptoms of acute low-metabolism, I don't think eating a lot of vitamin A is advisable. One meal of liver may have great benefits, because it comes with so many other beneficial compounds to metabolize the vitamin A, but it should be very occasional.

I've gone through the whole experience and it really seems like real pro-vitamin A needs increase in lockstep with metabolism. Small daily amounts of vitamin A, from good grass-fed butter, cream etc. are good but liver is really a food which is more beneficial when metabolism is rev'ed up and the stores of vitamin A are quickly metabolized into the steroid hormones.

Based on my current understanding, children and teenagers probably can benefit immensely from regular liver consumption. Any presence of persistent acne in teenagers is a good indication of the need for liver. Sunshine is also very important. I think optimizing those things in development is one of the most important things a parent can do for their children, because it sets them up for much greater metabolic health moving forward.

If you're cold all the time, and hypothyroid, the vitamin A just accumulates I think, and considering its role in cell division and skin shedding, it's no wonder the dry skin, eyes etc. and the other symptoms you mention are common. Anecdotally, I experienced dry eyes for a full year after eating a lot of liver while severely hypothyroid.

Or do they continue to push on trying to deplete vitamin A with the expectation that great health will await them once they finally deplete their vitamin A stores? The latter approach is a dangerous one if it turns out that retinol is a vitamin after all, needed for healthy skin and vision. What if a person develops cataracts or other forms of eye-damage during the detox process?

I think a careful approach of using vitamin E, C is better than focusing on depleting vitamin A. Vitamins E and C are the body's fat-soluble and water-soluble antioxidants and in the literature they're shown to be able to prevent the oxidation of vitamin A. My understanding is that taking extra thyroid for a time can help ''empty'' the stores of vitamin A. But in general, a simple active lifestyle with plenty of sun exposure in the summer will do the same. The vitamin A requirements seem to increase as vitamin D levels go up, and with light exposure in general.


So it's clearly an interaction of several elements, and context is very important as usual.