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

[Tarmander]

When I was super stringent with vitamin A I seemed to have defiency symptoms while at the same time feeling much better. My brainfog was lessened dramatically, I slept better, I had better vision (night blindness disappeared among other things), eyes became white instead of reddish, and I think my temps were higher. But my skin got worse and worse, my digestion got more and more sensitive

This is exactly my experience as well. When I do very low vit A, many things improve, digestion seems to get more and more sensitive. Skin seems better though. Long term, bones strengthening and realigning is supposedly something to look forward to. I have a crooked finger I am watching

I think the theory of vitamin A detox as talked about often over on the blog forum is incorrect. "Detox" is always what every new health fad reaches to when it encounters issues because it preserves the theory while encouraging people to stick with it. I think it is much more likely the "detox" symptoms are really some biochemical reaction taking place that vitamin A was facilitating that is now gone, and causing problems. I have a hunch it is about cholesterol but I am not sure. @Amazoniac is showing throughout this thread how silly the idea of detox is, so something else is going on.

 

[postman]

This is exactly my experience as well. When I do very low vit A, many things improve, digestion seems to get more and more sensitive. Skin seems better though. Long term, bones strengthening and realigning is supposedly something to look forward to. I have a crooked finger I am watching

I think the theory of vitamin A detox as talked about often over on the blog forum is incorrect. "Detox" is always what every new health fad reaches to when it encounters issues because it preserves the theory while encouraging people to stick with it. I think it is much more likely the "detox" symptoms are really some biochemical reaction taking place that vitamin A was facilitating that is now gone, and causing problems. I have a hunch it is about cholesterol but I am not sure. @Amazoniac is showing throughout this thread how silly the idea of detox is, so something else is going on.

I'm still open to the idea of it being a detox reaction, I just don't know. I don't have a reflexive disdain for the concept of detox like so many in the medical mainstream have.

 

[Collden]

This is exactly my experience as well. When I do very low vit A, many things improve, digestion seems to get more and more sensitive. Skin seems better though. Long term, bones strengthening and realigning is supposedly something to look forward to. I have a crooked finger I am watching

I think the theory of vitamin A detox as talked about often over on the blog forum is incorrect. "Detox" is always what every new health fad reaches to when it encounters issues because it preserves the theory while encouraging people to stick with it. I think it is much more likely the "detox" symptoms are really some biochemical reaction taking place that vitamin A was facilitating that is now gone, and causing problems. I have a hunch it is about cholesterol but I am not sure. @Amazoniac is showing throughout this thread how silly the idea of detox is, so something else is going on.

Did you try adding back some VA already?

 

[Terma]

@Amazoniac
Genetic deletion of Cyp26b1 negatively impacts limb skeletogenesis by inhibiting chondrogenesis

Cyp26b1, a retinoic acid (RA)-metabolising enzyme, is expressed in the developing limb bud, and Cyp26b1(-/-) mice present with severe limb defects. These malformations might be attributable to an RA-induced patterning defect; however, recent reports suggest that RA is dispensable for limb patterning. In this study, we examined the role of endogenous retinoid signalling in skeletogenesis using Cyp26b1(-/-) mice and transgenic mice in which Cyp26b1 is conditionally deleted under control of the Prrx1 promoter beginning at ~E9.5 (Prrx1Cre(+)/Cyp26b1(fl/fl)). We found that the limb phenotype in Prrx1Cre(+)/Cyp26b1(fl/fl) mice was less severe than that observed in Cyp26b1(-/-) animals and that a change in retinoid signalling contributed to the difference in phenotypes. We systematically examined the role of endogenous RA signalling in chondrogenesis and found that Cyp26b1(-/-) cells and limb mesenchymal cells treated with a CYP inhibitor, are maintained in a pre-chondrogenic state, exhibit reduced chondroblast differentiation and have modestly accelerated chondrocyte hypertrophy. Furthermore, Cyp26b1(-/-) mesenchyme exhibited an increase in expression of genes in a closely related tendogenic lineage, indicating that retinoid signals in the limb interfere with differentiation and maintain progenitor status. Together, these findings support an important function for RA in regulating the behaviour of mesenchymal progenitors, and their subsequent differentiation and maturatio

Retinoid signalling has been shown to be required to promote the transition from prehypertrophy to hypertrophy during endochondral ossification in the developing limb (Koyama et al., 1999). Congruent with this, we have demonstrated that Cyp26b1 –/– cells, with the exception of Ptrhp and Ihh , exhibit modest changes in the expression of hypertrophic-associated markers. The small decrease in Col10 , Alp1 and Mmp13 expression and the delay in mineralisation probably result from the decrease in chondrogenic differentiation and the formation of fewer, albeit larger, cartilage nodules. Consistent with this, alkaline phosphatase staining around individual nodules is comparable between Cyp26b1 + and Cyp26b1 -null cultures.

Growth plates sustain skeletal growth through the proliferation of chondrocytes, matrix synthesis and accumulation, and chondrocyte hypertrophy. The growth plate is generally divided into two zones, the upper zone, which contains immature chondrocytes, maintained by PTHrP signalling, and the lower zone, which contains Ihh -expressing prehypertrophic and maturing hypertrophic chondrocytes. PTHrP regulates the expression of Ihh , which controls chondrocyte proliferation and maturation, and Ihh in turn regulates Pthrp expression, creating a feedback system that controls the growth of skeletal elements (Kronenberg, 2006). The hypertrophic portions of the growth plate have been shown to contain higher levels of endogenous retinoid signalling than the upper, immature zones and a requirement for RAR-mediated repression in the upper growth plate zone has been shown to maintain chondrocyte function and the production of cartilage- associated extracellular matrix proteins (Williams et al., 2010; Williams et al., 2009). Previous studies have also suggested that RA-mediated repression of target gene expression in the upper zone is necessary to maintain physiological levels of Ihh expression (Koyama et al., 1999). We demonstrate in this study that an increase in retinoid signalling substantially decreases Ihh expression. Consequently, hypertrophic chondrocytes emerge earlier, with less growth having occurred, and this might partly explain the observed truncation of skeletal elements. The role of RA upstream of Ihh is further exemplified by the striking resemblance between Cyp26b1 –/– and Ihh –/– limbs (St-Jacques et al., 1999). Our findings indicate that RA negatively impacts chondrogenesis before activation of Ihh signalling; however, RA appears to promote subsequent steps involving chondrocyte hypertrophy.

Regulation of retinoic acid distribution is required for proximodistal patterning and outgrowth of the developing mouse limb. - PubMed - NCBI

RA seems to control the speed of the cell cycle of chondrocytes from immature to fully-differentiate ones, or at least between pre-hypertrophy and hypertrophy and then transition to differentiation (resource sufficiency) as well as to apoptosis (resource shortfall due to growth factor dependency and/or other).

In other words, RA spins the cell cycle and determines the health of the resulting cells, like a gatekeeper: it grows healthy cells but helps terminate unhealthy ones and unchecked growth. Too much RA tends to stall growth, but not in all cases, not least due to the complexity of our limbs. It matches the classical view that RA generally aims for a stable differentiated state, even if it promotes some growth to get there.

This means that: in disease states of decreased proliferation (non-immune), RA may impede recovery even whether or not it is in excess (but obviously worse in excess, unless the other factor is worse); in disease states of excessive proliferation, RA can be useful as a pharmacological therapy and may be deficient; but the state in which high RA signaling is meant to be safe and good or signal for is the state of good health - sufficient resources and sufficient cell proliferation and growth - because RA helps you achieve faster and maintain your state, whatever that may be (with some complications along the immune system). It becomes harder to heal as we age and lose growth hormone, which is coincidentally involved with cartilage and joint repair. As an adult, you want growth hormone or some (partial) stand-in like DHEA, along with all cofactors involved in RA synthesis including NAD.

If things are growing, RA helps them finish sooner; otherwise it maintains the state you're currently in[, unless you so far as to trigger apoptosis via p53 and friends] - with possible exceptions for the immune system, where it gets complicated: in principle CYP26 while processing RA may lower available NADPH for other pathways, leading to lower kynurenine monooxygenase (KMO) since it requires NADPH, increasing kynurenine, which stimulates T-cells and can lead to autoimmunity (in addition, kynurenine interferes with muscle growth because it cannot fully substitute for tryptophan yet participates in that signaling anyway - high kynurenine and low tryptophan stalls growth of muscle cells). This may completely explain L-methylfolate's success: it can help regenerate NADPH as well as oppose the effects of RA on GNMT (growth hormone also does this) and allow methylation to increase - all of which counters RA. Coincidentally, carnitine (a heavily methylated product) is important to chondrocyte and other structural cell proliferation because it allows them to grow slowly but surely on a substrate of fat during the night. That's the time of day when the skeleton has the most leeway to grow, but it seems unlikely it can do it on carbs alone because the liver has to feed the brain all throughout the night (which you can partially offset with ketones). In a natural setting you need methylation to temporarily help make tissues especially skeletal more dependent on fat for slow but sufficient nighttime growth.

(Several links omitted because I already posted them once or more)

[On top of that, NADPH itself is known to participate in fatty acid and cholesterol synthesis, so very high RA may drain NADPH and wreck both and even other anabolic pathways; one theoretical consequence of this is a deficiency of lipid rafts, used in immune defense]

 

[Louise]

This is exactly my experience as well. When I do very low vit A, many things improve, digestion seems to get more and more sensitive. Skin seems better though. Long term, bones strengthening and realigning is supposedly something to look forward to. I have a crooked finger I am watching

I think the theory of vitamin A detox as talked about often over on the blog forum is incorrect. "Detox" is always what every new health fad reaches to when it encounters issues because it preserves the theory while encouraging people to stick with it. I think it is much more likely the "detox" symptoms are really some biochemical reaction taking place that vitamin A was facilitating that is now gone, and causing problems. I have a hunch it is about cholesterol but I am not sure. @Amazoniac is showing throughout this thread how silly the idea of detox is, so something else is going on.

What do you think is happening to people on the low A diet who report feeling significantly more ill after sun exposure?

 

[Soren]

I assume that @haidut has opined on this theory of vitamin a toxicity? If someone could direct me to his view that would be appreciated.

I have to say I am not convinced either way at the moment. For my own part I have always noticed a reduction in acne when I've used topical vitamin A palmitate.

 

[postman]

I assume that @haidut has opined on this theory of vitamin a toxicity? If someone could direct me to his view that would be appreciated.

I have to say I am not convinced either way at the moment. For my own part I have always noticed a reduction in acne when I've used topical vitamin A palmitate.

If you click the search bar in the upper right you can also click the checkbox for searching this thread only, and comments by specific users only. If I recall correctly his comments were about as arrogantly dismissive as Ray's.

 

[Soren]

If you click the search bar in the upper right you can also click the checkbox for searching this thread only, and comments by specific users only. If I recall correctly his comments were about as arrogantly dismissive as Ray's.

Oh wow I actually didn't know you could do that for specific threads. Thanks! Man can't believe I've gone this long on the forum without the ability to use that.

 

[Tarmander]

What do you think is happening to people on the low A diet who report feeling significantly more ill after sun exposure?

Happened to me, so I am not sure. I am looking at cholesterol, vitamin D, sunlight causing lowering of cholesterol and production of cholesterol sulfate perhaps, and how vitamin C and A fit into that. I will let you know if I find anything.

Did you try adding back some VA already?

I have days where I get around 1000 IU and I do not really notice to be honest. I have yet to try liver or a large dose ala 10k IU

I'm still open to the idea of it being a detox reaction, I just don't know. I don't have a reflexive disdain for the concept of detox like so many in the medical mainstream have.

I am open to it as well...in fact I would love for it to be true but I am ready for things to be harder.

 

[gaze]

has anyone looked into low b12 connection to excess beta carotene? for me, stress and poor diet wrecked my gut, my b12 dropped, got yellowish skin, so i think it all has to do with low stomach acid>no b12 absorption>poor regulation of carotene>vit A deficiency/excess symptoms. Of course, there’s something to be said about high dose retinol and liver and the role that plays, but there’s definitely a gut/liver utilization of vit A that’s a problem

 

[BigChad]

has anyone looked into low b12 connection to excess beta carotene? for me, stress and poor diet wrecked my gut, my b12 dropped, got yellowish skin, so i think it all has to do with low stomach acid>no b12 absorption>poor regulation of carotene>vit A deficiency/excess symptoms. Of course, there’s something to be said about high dose retinol and liver and the role that plays, but there’s definitely a gut/liver utilization of vit A that’s a problem

how would you say one could get out of the low stomach acid trap? seems like once you get it, it becomes a cycle where you maintain the low stomach acid state. other than taking thyroid/t3 itself, are there supplements or dietary changes you can make to promote more stomach acid production. other than taking hcl or vinegar supplements. It seems like although zinc, b vitamins, iron, phosphorus etc increase stomach acid, if they aren't getting absorbed due to low stomach acid they won't be able to increase it?

 

[gaze]

how would you say one could get out of the low stomach acid trap? seems like once you get it, it becomes a cycle where you maintain the low stomach acid state. other than taking thyroid/t3 itself, are there supplements or dietary changes you can make to promote more stomach acid production. other than taking hcl or vinegar supplements. It seems like although zinc, b vitamins, iron, phosphorus etc increase stomach acid, if they aren't getting absorbed due to low stomach acid they won't be able to increase it?

For me i’ve noticed the best thing to do is to eat a lot of calories, mainly non liquid. Eating more food forces your body to produce more stomach acid to digest more food. one may have to eat through reflux until your body produces more acid. This part is very important. To cure yourself of this you have to be ready to deal with gas/bloating/horrible feeling, and just keep eating until your body normalizes. Also, low-fat, low-carb,low protein are all bad. Eat a lot of everything so ur body knows it doesn’t need have to worry about getting certain things. No matter what, never take anti-acids and even things like baking soda should be avoided because it’s alkaline. In certain starvation experiments, they found deficiencies in b vitamins, zinc or whatever it may be will NOT fix themselves with supplementation combined with too few calories. I think one just has to eat a ton of food until the body starts producing more stomach acid and holds onto minerals/vitamins. with age, stomach acid production goes down, but calorie consumption is almost always reduced as one gets very old, probably because lower thyroid, low appetite, etc

 

[dwide]

Hey guys been a while since I had any updates. I have been going through severe TMD on my right side. Been on ibuprofen twice a day for two months. And can't chew very easily as I'm now missing a chewing molar on the other side. So it's been extremely difficult to go low vitamin A. My main foods are full fat Greek yogurt for the calories and nutrition, bananas, ice cream, some cheese, pasta, and mashed potatoes. I'm also drinking some coffee lately. Wellllllll TMJ is still very very sore and I'm running out of ideas. It is worse at the end of my cycle. Progesterone flared it up to a level 9 when I took it for pregnancy prevention one day so I haven't taken that at all. Other than that I'm doing very well. But I think the Greek yogurt is not helping. What could I eat that is lower in vitamin A that isn't tough to chew? Ground beef is completely out of the equation unless it's Taco Bell type processed. Anything I make at home flares me up quite severely as it's using the chewing muscles too much.

Haven't read through the rest of the thread, so some of these may have been addressed, but some suggestions off the top of my head:
* You could try replacing butter with pastured lard. It has a much more mild taste than tallow. I use the leaf lard, almost no pork flavor, I get it from a local farm but you can buy online too (just more expensive). I've been doing this recently, adding it to mashed potatoes and such, and it's going well. I intend to try it on sourdough bread too. I know some people on the low VA thing aren't big on pork but I've had no issues -- for me it's noticeably better than butter.
* I've been making a cornbread with white masa harina. Very calorie dense and delicious. Masa, lard, sugar, bob's skim milk powder, egg white, salt, baking powder, water. If you add more water and cook it in a pot maybe it'd turn into some kind of porridge?
* Unfortunately WRT meat/protein I don't know what to say. I've found that getting enough animal protein every day is important, but whole cuts of meat digest better than pre-ground. Maybe a pressure cooker and cook it to death? Or maybe grind it yourself in a food processor? (I intend to try this too because it's cheaper than steaks.)
* I've been eating Enjoy Life chocolate chips after meals if I feel like I need more calories. Maybe you could melt them down a bit? Dip bananas in it? They're not the best because cocoa fiber doesn't agree with me very well, and I seem to remember you saying you can't do much fiber either. I might replace them with a homemade chocolate that's mostly cocoa butter+sugar with a tiny bit of cocoa powder + vanilla for taste.

 

[dwide]

You should consider Gerolsteiner mineral water, it’s easily found in stores. and it has 350 mg per liter, i’m surprised no one talks about mineral water as a source of calcium. I bet the water from lakes and rivers which people drank from 2000 years ago were crazy high in minerals, due to good natural soil.

I mentioned mineral water a while back, during a previous iteration of calcium discussion, but it got buried.

Gerolsteiner gives me headaches, possibly the bicarbonates. YMMV, but I prefer San Pellegrino, not as much calcium (about half as much), but I think it tastes better and it's cheaper too. Also high in sulfate, which is supposedly important (see Stephanie Seneff).

Just a thought, those with hard water may not need to worry about calcium at all.

 

[Louise]

Haven't read through the rest of the thread, so some of these may have been addressed, but some suggestions off the top of my head:
* You could try replacing butter with pastured lard. It has a much more mild taste than tallow. I use the leaf lard, almost no pork flavor, I get it from a local farm but you can buy online too (just more expensive). I've been doing this recently, adding it to mashed potatoes and such, and it's going well. I intend to try it on sourdough bread too. I know some people on the low VA thing aren't big on pork but I've had no issues -- for me it's noticeably better than butter.
* I've been making a cornbread with white masa harina. Very calorie dense and delicious. Masa, lard, sugar, bob's skim milk powder, egg white, salt, baking powder, water. If you add more water and cook it in a pot maybe it'd turn into some kind of porridge?
* Unfortunately WRT meat/protein I don't know what to say. I've found that getting enough animal protein every day is important, but whole cuts of meat digest better than pre-ground. Maybe a pressure cooker and cook it to death? Or maybe grind it yourself in a food processor? (I intend to try this too because it's cheaper than steaks.)
* I've been eating Enjoy Life chocolate chips after meals if I feel like I need more calories. Maybe you could melt them down a bit? Dip bananas in it? They're not the best because cocoa fiber doesn't agree with me very well, and I seem to remember you saying you can't do much fiber either. I might replace them with a homemade chocolate that's mostly cocoa butter+sugar with a tiny bit of cocoa powder + vanilla for taste.

G. Smith says there is significant vitamin A in pork fat. Some refer to it as the "lard factor".

 

[dwide]

G. Smith says there is significant vitamin A in pork fat. Some refer to it as the "lard factor".

Garrett $mith disables right-click on text. For such a low integrity move, I question anything he says. (Half-joking.)

But seriously, I feel good when I eat lard. So I've been eating it. I really don't have a stance on the whole "vitamin A is toxic" idea. I'm just after results. A strict vitamin A elimination diet didn't work for me, so I've kept what was useful and discarded the rest.

 

[Vinero]

If you click the search bar in the upper right you can also click the checkbox for searching this thread only, and comments by specific users only. If I recall correctly his comments were about as arrogantly dismissive as Ray's.

And also Chris Masterjohn, who referred to us (the low-vitamin A people) as the "flat earthers of the nutrition world" or something. Gee, thanks for pointing out our positive testimonials about the low-vitamin A diet don't mean anything. This reminds me of when Ray talked about how when he was following Biology classes he was doing some experiments of studying the behavior of cells. When they observed a behavior of cells that wasn't in agreement with the textbook behavior of cells the professors would just pretend they didnt see it. Ofcourse these nutrition-gurus aren't going to admit the vitamin A they have been recommending or selling to people for years could have harmed their clients and followers. By the way, I still haven't seen any of these nutrition-gurus debunk the work of Grant Genereux. They simply dismiss the vitamin A toxicity theory as being too far out there.

 

[Vinero]

Below is haidut's response in this thread. His short response really destroys Grant Genenereux' work of 800+ pages in one sentence! (sarcasm)

Grants work:
https://ggenereux.blog/wp-content/uploads/2016/10/extinguishing-the-fires-of-hell2.pdf
https://ggenereux.blog/wp-content/uploads/2018/09/PoisoningForProfits.pdf

Vinero said:
"Are you going to continue to ignore this topic @haidut? Please stop selling estroban and retinil.
Start your research in how to stimulate the detoxification of vitamin A. Please make Idealabs dedicated to tackle vitamin A toxicity."

Haidut said:
"Lol, you crack me up with your stuff.
A random thread claiming toxicity for one of the most important nutrients out there, by a person who ostensibly cured himself by restricting this one nutrient. No evidence except that one person's report. Wow, I am overwhelmed. /s
So, you think I should take this over the hundreds of large human studies showing no toxicity from hundreds of thousands IU vitamin A daily, and another 20-30 studies showing solid NOAEL of about 25,000 IU daily? And stop selling EstroBan which has a meager 6,000 IU per serving or Retinil which has 2,000 IU - 5,000 IU per drop?? Based on nothing else but this "evidence"??
Did you email Walmart, Amazon and the 10,000+ other vendors selling vitamin A and ask them to stop selling it as well? In case you have not noticed, buying is voluntary. If somebody thinks vitamin A does not sit well with them then they are free to not buy any product containing it. Until I see real evidence that vitamin A is dangerous and is an actual cause of even one chronic condition there is not much to say or do on this topic."

Notice he doesn't actually explain why the vitamin A toxicity theory is wrong. He also simply ignores the real-world experiences of people healing their auto-immune diseases like eczema. Not only Grant has cured himself, but many others have including myself. You can find the positive testimonials scattered throughout this thread, on Grants' forum, and here: Testimonials / Anecdotes / Recoveries from doing the Poison/"Vitamin A" and Glyphosate Detox
Haidut talks about the scientific studies he has read that show no toxicity from vitamin A, but Dr Garret Smith has done really good work of finding tons of studies about the toxic effects of vitamin A, which he posts on the blog forum of nutritionrestored.com. Have a look there and see that the evidence that vitamin A is toxic absolutely exists:
START HERE...Summary, Grant's books, the "rules", the misconceptions, the falsehoods
Conditions / Diseases / Syndromes caused by Poison/"Vitamin A"
Case studies / poisonings / observations about Poison/"Vitamin A" causing poor health and disease
Are we being purposely poisoned with Poison/"Vitamin A"? Interesting coincidences...

 

[Collden]

@Amazoniac is showing throughout this thread how silly the idea of detox is, so something else is going on.

That's a strong word. How, specifically, has he shown that the idea of detox is silly? I think this theory is one where the idea of detox actually makes good sense and is well supported by clinical observations. That is - there are numerous cases where people who've taken large amounts of VA have symptoms of toxicity and dysregulated VA metabolism for a long time after VA is minimised, in some cases symptoms only begin some time after discontinuation. In some cases "detox" symptoms may rather be symptoms of healing the damage from toxicity.

Massive vitamin A intoxication with ascites and pleural effusion. - PubMed - NCBI
"Vitamin A intoxication was diagnosed in a 14-year-old girl who presented with massive exudative ascites and right pleural effusion, impaired liver enzymes, and hypertriglyceridemia. Electron microscopy of liver biopsy material demonstrated numerous perisinusoidal lipid-filled Ito cells. The patient had taken 100-200,000 I.U. vitamin A per day for 15 months. Serum vitamin A level remained elevated for 4 months after vitamin discontinuation. The unusual severity of portal hypertension was documented by a high wedged hepatic vein pressure level. The ascites occurred 2 months after vitamin A had been discontinued, probably owing to particularly slow mobilization of large hepatic stores of vitamin A. Portal hypertension disappeared after a 6-month low vitamin A diet, but the liver biopsy failed to demonstrate any decrease in number or size of Ito cells, suggesting that lipid venous obstruction is unlikely to be the only mechanism responsible for portal hypertension in vitamin A-induced liver disease."

Vitamin A intoxication presenting with ascites and a normal vitamin A level.
- "Vitamin A intake was minimized. After eight weeks of therapy the patient experienced worsening dermatitis, fissured lips, increased hair loss, irritability, and tenderness of the extremities"

- "It was only after the child received nutritional supplementation (with minimal vitamin A intake) that her serum vitamin A level rose into a clearly toxic range"

- "Although the vitamin A supplementation had been stopped month before admission, the child's condition worsened with the development of overt ascites. It has been proposed that this delay in the onset of ascites is due to the effects of high-dose vitamin A administration on the liver, which appears to result in enlarging and transforming the Ito cells. The enlargement caused by vitamin A in these cells decreases the sinusoidal spaces. Later, fibroblastic transformation of the Ito cells leads to a fibrocongestive hepatic lesion and ascites. This is presumed to be a dose- and time-related phenomenon and may not lead initially to enlargement of the liver."

Severe hypervitaminosis A in siblings: evidence of variable tolerance to retinol intake. - PubMed - NCBI
"The patient's intake of vitamin A was restricted to <300 IU/day. For a subsequent year serum retinol levels remained normal, and retinyl ester levels remained markedly elevated, with occasional wide fluctuations (Fig. 1). Episodic otitis, sepsis, hepatomegaly, and hypercalcemia occurred, and increased intra- cranial pressure persisted. Clinical features of vitamin A intoxication corresponded with relative increases in circulating retinyl ester values."

Hepatic hypervitaminosis A: a familial observation. - PubMed - NCBI
"Four siblings with hepatic fibrosis are described. The liver damage in these patients was secondary to chronic ingestion of massive doses of vitamin A for congenital ichthyosis. Although the extrahepatic manifestations were helpful in the diagnosis of hypervitaminosis A, the distinctive features of hepatic histopathology were confirmatory. The plasma concentrations of vitamin A and retinol-binding protein were misleading. The recovery from the liver damage in these patients was slow despite a complete withdrawal of the vitamin A intake. These cases show the importance of hepatic vitamin A assessment in the diagnosis of hepatic fibrosis."

 

[gaze]

That's a strong word. How, specifically, has he shown that the idea of detox is silly? I think this theory is one where the idea of detox actually makes good sense and is well supported by clinical observations. That is - there are numerous cases where people who've taken large amounts of VA have symptoms of VA toxicity and dysregulated VA metabolism for a long time after VA is minimised, in some cases symptoms only begin some time after discontinuation. In some cases "detox" symptoms may rather be symptoms of healing the damage from toxicity.

Massive vitamin A intoxication with ascites and pleural effusion. - PubMed - NCBI
"Vitamin A intoxication was diagnosed in a 14-year-old girl who presented with massive exudative ascites and right pleural effusion, impaired liver enzymes, and hypertriglyceridemia. Electron microscopy of liver biopsy material demonstrated numerous perisinusoidal lipid-filled Ito cells. The patient had taken 100-200,000 I.U. vitamin A per day for 15 months. Serum vitamin A level remained elevated for 4 months after vitamin discontinuation. The unusual severity of portal hypertension was documented by a high wedged hepatic vein pressure level. The ascites occurred 2 months after vitamin A had been discontinued, probably owing to particularly slow mobilization of large hepatic stores of vitamin A. Portal hypertension disappeared after a 6-month low vitamin A diet, but the liver biopsy failed to demonstrate any decrease in number or size of Ito cells, suggesting that lipid venous obstruction is unlikely to be the only mechanism responsible for portal hypertension in vitamin A-induced liver disease."

Vitamin A intoxication presenting with ascites and a normal vitamin A level.
- "Vitamin A intake was minimized. After eight weeks of therapy the patient experienced worsening dermatitis, fissured lips, increased hair loss, irritability, and tenderness of the extremities"

- "It was only after the child received nutritional supplementation (with minimal vitamin A intake) that her serum vitamin A level rose into a clearly toxic range"

- "Although the vitamin A supplementation had been stopped month before admission, the child's condition worsened with the development of overt ascites. It has been proposed that this delay in the onset of ascites is due to the effects of high-dose vitamin A administration on the liver, which appears to result in enlarging and transforming the Ito cells. The enlargement caused by vitamin A in these cells decreases the sinusoidal spaces. Later, fibroblastic transformation of the Ito cells leads to a fibrocongestive hepatic lesion and ascites. This is presumed to be a dose- and time-related phenomenon and may not lead initially to enlargement of the liver."

Severe hypervitaminosis A in siblings: evidence of variable tolerance to retinol intake. - PubMed - NCBI
"The patient's intake of vitamin A was restricted to <300 IU/day. For a subsequent year serum retinol levels remained normal, and retinyl ester levels remained markedly elevated, with occasional wide fluctuations (Fig. 1). Episodic otitis, sepsis, hepatomegaly, and hypercalcemia occurred, and increased intra- cranial pressure persisted. Clinical features of vitamin A intoxication corresponded with relative increases in circulating retinyl ester values."

Hepatic hypervitaminosis A: a familial observation. - PubMed - NCBI
"Four siblings with hepatic fibrosis are described. The liver damage in these patients was secondary to chronic ingestion of massive doses of vitamin A for congenital ichthyosis. Although the extrahepatic manifestations were helpful in the diagnosis of hypervitaminosis A, the distinctive features of hepatic histopathology were confirmatory. The plasma concentrations of vitamin A and retinol-binding protein were misleading. The recovery from the liver damage in these patients was slow despite a complete withdrawal of the vitamin A intake. These cases show the importance of hepatic vitamin A assessment in the diagnosis of hepatic fibrosis."

well when a pale thin sickly looking vegan youtuber claims every single problem is stemmed from detox, I and many others tend to view the idea of detox as an excuse for an inadequate diet. vit A is a bit more perplexing, but you asked why is the idea of detox silly, and it’s silly cause everyone seems to throw that word around to explain every problem without evidence. If evidence is provided like you and many others have done, then it is more realistic, but i still tend to be apprehensive of detoxing