Low Toxin Studies "Vitamin A" not needed for steroidogenesis, contrary to Peat's claim

[mosaic01]

In his new video, Danny Roddy briefly mentions the concept of vitamin A as a toxin, and his only counter-argument is the claim that it's required for steroid production, and here he is echoing one of the arguments Ray Peat made in favor of the essentiality of retinol.

Ray Peat quotes:

"In animals, cholesterol is the basic sterol molecule, which is massively converted into other substances, including the steroid hormones. Thyroid hormone and vitamin A are required for this conversion."

"Although one of the important functions of vitamin A is its involvement in the formation of the steroids pregnenolone and progesterone (both of which moderate the effects of cortisol), it also has some hormone like actions directly on the cells of the immune system, and it stimulates production of interleukin-2 and both inhibits generation of specific suppressor cells and limits the intensity of activation of suppressor cells."

"If thyroid and vitamin A can’t be used efficiently to form steroids, a steroid imbalance is likely."

"to a very great extent, progesterone could substitute for vitamin A, meaning that a very large fraction of the vitamin A used by the body is used up in making progesterone, from which the other steroid hormones are made."

"Yes, it's definitely hard to get them coordinated when there's an imbalance in one direction or the other. For several years, when I had an extremely high metabolic rate, I needed 100,000 units per day during sunny weather to prevent acne and ingrown whiskers, but when I moved to a cloudy climate, suddenly that much was too much, and suppressed my thyroid. The average person is likely to be hypothyroid, and to need only 5,000 units per day."

Ray Peat is wrong when it comes to the involvement of retinol in steroid production. This concept has been gained from faulty rat studies.

Earlier in the Grant Genereux thread, @youngsinatra shared the following paper:

Vitamin A: Not Required for Adrenal Steroidogenesis in Rats​

Previous work supporting the vitamin A dependency of adrenal function in rats neglected to take into account a secondary effect of the deficiency, a decrease in hepatic ascorbic acid biosynthesis. Vitamin A-depleted rats maintained on a diet free of ascorbate had a decrease in the activity of adrenal 3 β-hydroxysteroid dehydrogenase, and extensive adrenocortical degeneration. The use of an ascorbate supplement prevented the symptoms. The results suggest that previous evidence for direct involvement of vitamin A in steroidogenesis may have been due to the production of a secondary deficiency, a chronic scorbutic condition.

The vitamin A dependency of steroidogenic organ function in rats has remained a controversial subject. Both adrenal (1, 2) and gonadal (3) dysfunction have been reported in hypovitaminosis A. Attempts have been made to apply this theory as an explanation for the apparent anticarcinogenic effects of vitamin A. Light (4) has proposed the existence of subclinical vitamin A deficiencies which result in decreased adrenocortical output. The correction of such a condition in a patient with cancer would be the equivalent of steroid therapy. In addition, Van Thiel et al. (5)have shown that ethanol interferes with testicular vitamin A metabolism, and they theorized that this could account for the occurrence of sterility in alcoholics. However, no attempt has been made to reconcile these theories with recent work that does not support the involvement of vitamin A in steroidogenesis (6, 7). A review of this field revealed that none of the investigators who attempted to produce a hypovitaminosis A condition (1-3, 6, 7) noted an important effect of hypovitaminosis A in the rat, a reduction in the hepatic biosynthesis of ascorbic acid (8). An examinationof the diets used indicated that in those experiments where significant steroidogenic dysfunction was noted both vitamins A and C were lacking in most of the reported diets (1-3). In one of the experiments that failed to support the aforementioned work(7), significant amounts of ascorbic acid were present in the diet (9). In another report (6) showing the absence of adrenal effects in vitamin A deficiency, no vitamin C was in the reported diet; but retinoic acid was used to deplete the vitamin A stores,and was then abruptly withdrawn. The effect of this regimen on the hepatic ascorbic acid synthesizing enzyme, gulonolactoneoxidase, is not known.
(...) The result of the reduction in ascorbic acid biosynthesis is a decrease in the activity of adrenal 3,-HSD, and a series of histological changes in the adrenal which resemble scurvy in the guinea pig (23, 24).These changes have been attributed to the vitamin A dependency of adrenocortical function (1, 2). The use of an ascorbate supplement in vitamin A-depleted rats prevented all of the aforementioned symptoms.The above data provide a possible explanation for the conflicting reports concerning the effects of hypovitaminosis A on the adrenal cortex of the rat; that is, a lack of vitamin C in their diet. Further work is needed to ascertain whether the "protective" effect of ascorbic acid is still present in more extreme cases of vitamin A-deficiency. However, our work shows the importance of ascertaining that only one deficiency exists when performing vitamin depletion studies.

As the paper from 1976 notes, "The use of an ascorbate supplement in vitamin A-depleted rats prevented all of the aforementioned symptoms."

The authors write that the idea for retinol being essential for steroid synthesis is a "controversial suject". It was (and is) by no means a settled thing within academia, but the discussion around this has probably been suppressed or ignored since the 80s.

From this data it becomes clear that the true issue here is simply a lack of ascorbic acid (in the context of diet-induced toxicity or nutrient deficiency), which we know is an anti-toxin.

So the argument that vA is essential for steroid synthesis seems to have no solid foundation. Danny Roddy is just copying Ray's claims without any critical reception here. If this is his best argument, it shows he has not seriously looked into the low A approach at all.

It would be helpful for many people if Danny Roddy, and others involved, would stop treating Ray Peat like he was infallible. There are many things he got outright wrong, and he was never questioned on these things by his followers. Ray Peat, like many other scientists of the 20th century, was blinded by the newly established vitamin ideology - the idea that we need to take in lots of chemicals in exactly the right amount to be healthy, as if life is some kind of complicated puzzle to solve. A concept that is opposite of the actual truth: We need to merely stop the ingestion of toxins and the body brings back itself into balance and health. Some of those toxins are even wrongly classified as essential in large amounts, and thus act as trojan horses for an absurd level of toxicity in our culture in present times.

 

[Peater]

Interesting. I pondered this very point here:

Does Garrett approach estrogen as a potential problematic hormone? I assume if the liver is working efficiently it can more easily deal with it.

One other thought I had is that vitamin A is 'needed' for pregnenolone synthesis, but Ray supplemented pregnenolone (The pictures from one of his books or newsletters show the improvements) but either supplemented A or ate foods high in it. There's a bit of a contradiction there, or I am missing something.

 

[FitnessMike]

There are many things he got outright wrong,

and there are many things that you probably are getting wrong? will be getting wrong in the future? you were also probably getting the wrong things in the past?

many things thought as 100% truths(to these people) will probably turn out to be wrong, or partially wrong.

People's truths are different, there simply is no one truth, your truth about things will change with time.

 

[mosaic01]

and there are many things that you probably are getting wrong? will be getting wrong in the future? you were also probably getting the wrong things in the past?

Indeed, that's why no one should blindly believe a single authority figure like Ray Peat. Unfortunately, Danny Roddy and others have never challenged Peat. Even in light of absurd ocurrences like Peat's teeth falling out within a week when he couldn't get milk quickly enough in Mexico, or strange concepts that do not make sense on first sight (people needing large amounts of calcium from milk even though the majority of the world population lives just fine without).

It's not possible to get everything right, but that's why people exchange ideas, and I am starting this thread to make Danny Roddy aware of his misconception in regards to steroidogenesis, and invite him to find better arguments in favor of vitamin A, or ideally, make him realize that there is a mass poisoning going on and retinol needs to be restricted for health.

Since this steroid argument has always been one of the central arguments Peat used to promote retinol, criticizing this concept can hopefully make some Peat followers wake up to the possibility that things are different than they have believed all of those years.

 

[Peater]

ocurrences like Peat's teeth falling out within a week when he couldn't get milk quickly enough in Mexico

I thought that was due to him experimenting with wheat bran on a long term basis as a cheap protein - it was only when he lost teeth he realised something was wrong.

 

[mosaic01]

I thought that was due to him experimenting with wheat bran on a long term basis as a cheap protein - it was only when he lost teeth he realised something was wrong.

Only thing I can find right now is this quote:

"My wheat germ experience related to decalcifying my teeth; at the time, in Mexico City, is was hard to get good milk."

I remembered a different quote, but I can't find the source right now. Maybe I got something confused here, not sure.

Edit: This is the post I remembered: Low Toxin Diet - Grant Genereux's Theory Of Vitamin A Toxicity

"he mentioned in a podcast how one of his teeth became very brittle and crumbled when he was in mexico and did not consume milk because he was not in the store early enough to get milk."

Not sure whether that refers to the same event. Would be nice to find that podcast.

 

[CLASH]

According to the research below vitamin A seems to have importance in the development of the testicles as well as the stimulation of cholesterols movement into the mitcohondria via StAR and the stimulation of the enzyme 17 alpha hydroxylase that adds hydroxyl groups to pregnenolone and progesterone to make other steroid hormones.

This would lend some credence to Danny and Dr. Peat's points about the importance of vitamin A in steroid hormone production.

Also, it focuses on other glandular tissues besides the adrenal gland, which possibly aren't as reliant on vitamin C as a cofactor.

Lastly, the research does mention the negative effects of an excess of vitamin A. This supports the idea of a "goldilocks zone" for vitamin A, where an excess is toxic but a deficiency is also harmful. I'm still reading Grant's work to find out where this goldilocks zone actually lies. I also wouldn't be surprised if the zone changes with different developmental periods in the lifespan.

"An excess of vitamin A leads to testicular lesions and spermatogenetic disorders, and a deficiency induces early cessation of spermatogenesis and adversely affects testosterone secretion. Furthermore, mice mutant for retinoic acid α receptors and retinoid X β receptors are sterile. Retinoids appear to exert an action on the
three main testicular types of cell (Sertoli, germinal and Leydig cells), as they act on the
signalling pathways and Sertoli cell metabolism, and modify numerous factors secreted in Sertoli cells. Retinoids also appear to be necessary for the proliferation and differentiation of A spermatogonia, and for spermiogenesis. In addition, vitamin A deficiency leads to atrophy of the accessory sex organs after decreased testosterone production. Recent studies have shown that retinoids already affect these three types of cell in fetuses. Curiously, the effects of retinoids on fetal and adult testis seem opposed."

Regulation and perturbation of testicular functions by vitamin A

In addition to playing a fundamental role in very diverse processes such as vision and the growth and differentiation of numerous types of cell, vitamin A (retinol) and its principal biologically active derivative, retinoic acid, are clearly involved in the regulation of testicular functions in...

rep.bioscientifica.com

"RA is a critical factor for the formation of the gonads in man and one of the major consequences of vitamin A deficiency apart from blindness is infertility (35, 76). In Leydig as well as ovarian cells, RA stimulates steroidogenic acute regulatory protein (StAR) and P450 17α-hydroxylase expression and thus steroidogenesis (77). The role of RA in the production of gonadic hormones of developed gonads appears less important although RA stimulates steroid hormone synthesis."

Vitamin A, endocrine tissues and hormones: interplay and interactions

Vitamin A (retinol) is a micronutrient critical for cell proliferation and differentiation. In adults, vitamin A and metabolites such as retinoic acid (RA) play major roles in vision, immune and brain functions and tissue remodelling and metabolism. This review presents the physiological...

ec.bioscientifica.com

 

[mosaic01]

Danny Roddy in the video I linked to brought forward a second reason why he rejects the anti-vitamin A stance. He says:

"Ray has been saying this forever... this is why it was kinda shocking to me that the vitamin A toxicity gained so much steam... Ray has been saying that vitamin A is highly unsaturated, in excess it suppresses the thyroid, so it has to be balanced with the thyroid."

It would not be shocking if he actually went to the source of the vitamin A toxicity movement and read Genereux' books, or watches his interviews. Because the central arguments don't resolve around what happens within the first hours of taking it, but the months and years afterwards - because it stays in the body.

This is common knowledge for scientists studying retinol and the reason vA is known to cause hepatotoxicity and teratogenicity in the first place. So this needs to be addressed. Talking about vA temporarily suppressing the thyroid is a strawman argument.

Roddy has said he suggests people go to the source of Ray Peat's own articles and podcasts to understand him. Well, the same is true for the problems of vitamin A - you need to listen to people who are advancing the knowledge in the field. In this case,

a) reading Grant Genereux for an overview, then going back to
b) learning about the scientifically established toxicity of retinol and
c) looking into the research by Anthony Mawson

is a good start.

The problem with vitamin A is not only that is is highly unsaturated, and thus degrades easily, the basic and fundamental problem, and the reason people suffer from chronic toxicity, is that retinol gets stored in the liver and in fat cells.

This means it does not matter how much thyroid you take with retinol, when you ingest a large amount, most of it will be stored away in the liver. Over time, when daily intake exceeds excretion, the liver will be filled up and highly toxic retinol and retinoic acid spills over into blood, organs and tissues. No one knows when this point is reached in a given person, but it is clear that the daily average excretion for many is lower than their intake. This is the fundamental problem with chronic toxicity. And getting that stuff out of the body is a lengthy process.

Chris Masterjohn has shown more knowledge of biochemistry and biology in his attempt to reply to Dr. Smith than Roddy, since he at least addresses the primary issue of long-term intake/storage and corresponding serum levels, but he also misses the point that chronic toxicity can happen even with very low levels of intake and the threshold for toxicity is both unknown and individually variable, but probably starts at "low" doses of 1500-3000 IU per day.

 

[Nick]

According to the research below vitamin A seems to have importance in the development of the testicles as well as the stimulation of cholesterols movement into the mitcohondria via StAR and the stimulation of the enzyme 17 alpha hydroxylase that adds hydroxyl groups to pregnenolone and progesterone to make other steroid hormones.

This would lend some credence to Danny and Dr. Peat's points about the importance of vitamin A in steroid hormone production.

Also, it focuses on other glandular tissues besides the adrenal gland, which possibly aren't as reliant on vitamin C as a cofactor.

Lastly, the research does mention the negative effects of an excess of vitamin A. This supports the idea of a "goldilocks zone" for vitamin A, where an excess is toxic but a deficiency is also harmful. I'm still reading Grant's work to find out where this goldilocks zone actually lies. I also wouldn't be surprised if the zone changes with different developmental periods in the lifespan.

"An excess of vitamin A leads to testicular lesions and spermatogenetic disorders, and a deficiency induces early cessation of spermatogenesis and adversely affects testosterone secretion. Furthermore, mice mutant for retinoic acid α receptors and retinoid X β receptors are sterile. Retinoids appear to exert an action on the
three main testicular types of cell (Sertoli, germinal and Leydig cells), as they act on the
signalling pathways and Sertoli cell metabolism, and modify numerous factors secreted in Sertoli cells. Retinoids also appear to be necessary for the proliferation and differentiation of A spermatogonia, and for spermiogenesis. In addition, vitamin A deficiency leads to atrophy of the accessory sex organs after decreased testosterone production. Recent studies have shown that retinoids already affect these three types of cell in fetuses. Curiously, the effects of retinoids on fetal and adult testis seem opposed."

Regulation and perturbation of testicular functions by vitamin A

In addition to playing a fundamental role in very diverse processes such as vision and the growth and differentiation of numerous types of cell, vitamin A (retinol) and its principal biologically active derivative, retinoic acid, are clearly involved in the regulation of testicular functions in...

rep.bioscientifica.com

"RA is a critical factor for the formation of the gonads in man and one of the major consequences of vitamin A deficiency apart from blindness is infertility (35, 76). In Leydig as well as ovarian cells, RA stimulates steroidogenic acute regulatory protein (StAR) and P450 17α-hydroxylase expression and thus steroidogenesis (77). The role of RA in the production of gonadic hormones of developed gonads appears less important although RA stimulates steroid hormone synthesis."

Vitamin A, endocrine tissues and hormones: interplay and interactions

Vitamin A (retinol) is a micronutrient critical for cell proliferation and differentiation. In adults, vitamin A and metabolites such as retinoic acid (RA) play major roles in vision, immune and brain functions and tissue remodelling and metabolism. This review presents the physiological...

ec.bioscientifica.com

The first paper partially relies on data from mice with mutant "retinoid receptors" but I think, as did Ray Peat, that cell "receptors" do not exist. Any experiment that relies on genetic mutations of receptors is junk science.

The rest of the conclusions about "vitamin A deficiency" appear to be based on other bad science, such as classifiying low blood retinol as a marker for vitamin-A deficient. In actuallity low blood retinol often means there is a protein and/or zinc deficiency preventing the body from making retinol binding protein. What happens then is the liver does not want to let go of stored retinoids because without RBP they are so dangerous, and retinol that gets into the blood without RBP gets turned into retinoic acid, which is not tested for when determining vitamin-A deficiency. This is why "deficient" people/animals (as determined by serum retinol level) are often actually the most retinoid-toxic.

 

[Apple]

Only thing I can find right now is this quote:

"My wheat germ experience related to decalcifying my teeth; at the time, in Mexico City, is was hard to get good milk."

I remembered a different quote, but I can't find the source right now. Maybe I got something confused here, not sure.

Edit: This is the post I remembered: Low Toxin Diet - Grant Genereux's Theory Of Vitamin A Toxicity

"he mentioned in a podcast how one of his teeth became very brittle and crumbled when he was in mexico and did not consume milk because he was not in the store early enough to get milk."

Not sure whether that refers to the same event. Would be nice to find that podcast.

I think he couldn't afford good food at that point (while living in mexico) and relied on tortillas ( they are high in calcium btw). He used to make wheat germ pancakes. I rather think it was lack of protein that made him lose some teeth. He probably couldn't afford meat.

UnGodly: The Passions, Torments, and Murder of Atheist Madalyn Murray O'Hair By Ted Dracos.
The whole chapter is dedicated to Ray Peat. It was in 1965.
Peat taught nutrition cources in mexico and made wheat-germ pancakes for his students attempting to get them on a more healthy diet.
Interestingly they mention niacin.
I bet he already knew about niacin/calcium in mexican nixtamalized tortillas.

 

[Peater]

I rather think it was lack of protein that made him lose some teeth. He probably couldn't afford

I didn't lose any teeth after a year and a half on a vegan diet. I don't have any fillings either.

 

[Apple]

I didn't lose any teeth after a year and a half on a vegan diet. I don't have any fillings either.

Vegan diet still can provide enough protein.
Maybe wheat germ and bran chelate calcium. Coupled with high citrus intake, who knows what else he did.
I just don't get it, what kind of nutrition science he taught in those times ?
Ok, it was hard to get "good milk". What does that even mean ? In 60th all milk was unadulterated with less vaccines for cows.
I hardly can believe he just lived on wheat germ and water... probably there was smth else in that story.

 

[Peater]

Ok, it was hard to get "good milk". What does that even mean ? In 60th all milk was unadulterated with less vaccines for cows

That's a good point. I wonder if he meant in terms of spoilage due to refrigeration not being as common.

I just don't get it, what kind of nutrition science he taught in those times ?

I'd be interested to know as well. It could be he just thought he'd found something no one else had realised, with no studies to warn of the impact.

I hardly can believe he just lived on wheat germ and water... probably there was smth else in that story

True, if teaching (a respectable profession then) had me in that position I would quit and go and work in a shop.

 

[CLASH]

The first paper partially relies on data from mice with mutant "retinoid receptors" but I think, as did Ray Peat, that cell "receptors" do not exist. Any experiment that relies on genetic mutations of receptors is junk science.

The rest of the conclusions about "vitamin A deficiency" appear to be based on other bad science, such as classifiying low blood retinol as a marker for vitamin-A deficient. In actuallity low blood retinol often means there is a protein and/or zinc deficiency preventing the body from making retinol binding protein. What happens then is the liver does not want to let go of stored retinoids because without RBP they are so dangerous, and retinol that gets into the blood without RBP gets turned into retinoic acid, which is not tested for when determining vitamin-A deficiency. This is why "deficient" people/animals (as determined by serum retinol level) are often actually the most retinoid-toxic.

Your first statement is not a rebuttle its an opinion, in particular the statement calling mutations of receptors "junk science". I think without further support or extension, this statement is largely irrelevant to the specific conversation at hand.

Retinol binding protein deficiency secondary to zinc deficiency or protein deficiency are possible causes, but to assume that this is the case in these situations is logically irresponsible.

It would be great to see some support for your statements so they can be verified. Even further it would be great to see all of these supposed "vitamin A toxic people" verify thier vitamin A toxicity. While I wouldn't rule out that there are peatarians who have possibly induced vitamin A toxicity through high dose vitamin A supplementation and liver intake, I'm not convinced that this is the boogeyman responsible for many peoples problems.

 

[CLASH]

Danny Roddy in the video I linked to brought forward a second reason why he rejects the anti-vitamin A stance. He says:

"Ray has been saying this forever... this is why it was kinda shocking to me that the vitamin A toxicity gained so much steam... Ray has been saying that vitamin A is highly unsaturated, in excess it suppresses the thyroid, so it has to be balanced with the thyroid."

It would not be shocking if he actually went to the source of the vitamin A toxicity movement and read Genereux' books, or watches his interviews. Because the central arguments don't resolve around what happens within the first hours of taking it, but the months and years afterwards - because it stays in the body.

This is common knowledge for scientists studying retinol and the reason vA is known to cause hepatotoxicity and teratogenicity in the first place. So this needs to be addressed. Talking about vA temporarily suppressing the thyroid is a strawman argument.

Roddy has said he suggests people go to the source of Ray Peat's own articles and podcasts to understand him. Well, the same is true for the problems of vitamin A - you need to listen to people who are advancing the knowledge in the field. In this case,

a) reading Grant Genereux for an overview, then going back to
b) learning about the scientifically established toxicity of retinol and
c) looking into the research by Anthony Mawson

is a good start.

The problem with vitamin A is not only that is is highly unsaturated, and thus degrades easily, the basic and fundamental problem, and the reason people suffer from chronic toxicity, is that retinol gets stored in the liver and in fat cells.

This means it does not matter how much thyroid you take with retinol, when you ingest a large amount, most of it will be stored away in the liver. Over time, when daily intake exceeds excretion, the liver will be filled up and highly toxic retinol and retinoic acid spills over into blood, organs and tissues. No one knows when this point is reached in a given person, but it is clear that the daily average excretion for many is lower than their intake. This is the fundamental problem with chronic toxicity. And getting that stuff out of the body is a lengthy process.

Chris Masterjohn has shown more knowledge of biochemistry and biology in his attempt to reply to Dr. Smith than Roddy, since he at least addresses the primary issue of long-term intake/storage and corresponding serum levels, but he also misses the point that chronic toxicity can happen even with very low levels of intake and the threshold for toxicity is both unknown and individually variable, but probably starts at "low" doses of 1500-3000 IU per day.

A quote directly from the Chris Masterjohn article you linked, where Chris discusses chronic toxicity dosages and links to a meta-analysis:

"According to the above-cited meta-analysis, the main risk factor for vitamin A toxicity arise months or years of consistently taking at least 165 IU per kilogram body weight per day, and in the majority of cases greater than 2300 IU per kilogram body weight per day. For a person weighing 70 kilograms (154 pounds), this is a minimum of 11,550 IU and higher than 161,000 IU per day in the majority of cases. These figures apply to cases where vitamin D was not supplemented alongside it.

When vitamin D is taken alongside vitamin A, the majority of vitamin A toxicity cases involve months or years of consistently taking more than 4620 IU vitamin A per kilogram body weight per day, which for a person weighing 70 kilograms is 323,400 IU per day."

 

[mosaic01]

This is why "deficient" people/animals (as determined by serum retinol level) are often actually the most retinoid-toxic.

That's why I suspect the "vitamin a depleted rats" in the steroidogenesis studies were actually the most toxic, and ascorbic acid acted protectively to prevent some of the consequences. Just as Grant Genereux always said.

A quote directly from the Chris Masterjohn article you linked, where Chris discusses chronic toxicity dosages and links to a meta-analysis:

"According to the above-cited meta-analysis, the main risk factor for vitamin A toxicity arise months or years of consistently taking at least 165 IU per kilogram body weight per day, and in the majority of cases greater than 2300 IU per kilogram body weight per day. For a person weighing 70 kilograms (154 pounds), this is a minimum of 11,550 IU and higher than 161,000 IU per day in the majority of cases. These figures apply to cases where vitamin D was not supplemented alongside it.

When vitamin D is taken alongside vitamin A, the majority of vitamin A toxicity cases involve months or years of consistently taking more than 4620 IU vitamin A per kilogram body weight per day, which for a person weighing 70 kilograms is 323,400 IU per day."

The meta-analysis looks for people with clinical toxicity. To be included in such a meta-analysis, the vA toxicity must be extreme.

"... that the following serum markers were most commonly elevated: retinol in 89% of cases, γ-glutamyltranspeptidase in 83%, lipids in 80%, triglycerides in 75%, alkaline phosphatase in 67%, prothrombin time in 53%, cholesterol in 50%, aspartate aminotransferase in 49%, bilirubin in 48%, and calcium in 46%. "

Retinol is only elevated in extreme cases when the body can't regulate the homeostasis anymore.

When Grant Genereux, Dr. Smith and people here talk about vA toxicity, they are usually talking about "subclinical" toxicity that is not measurable with the usual blood tests (except some tests that are not commonly used, like free retinyl esters). In other words, medicine is just looking at the wrong parameters to define toxicity. As usual, they take the most obvious/extreme cases and then exclaim everything else does not exist.

People who get chronically depressed, have hair loss, anxiety, sleep problems, chronic fatigue, etc. etc. from RDA levels of retinol, but don't match the above blood parameters will never be grouped under the term "vitamin A toxicity", even though they get healthy from stopping the vA intake.

It's just the usual vodoo witchcraft of modern medicine. First, they define the problem in a way to distort the truth, and then they can tell people that nothing is there and they are just making their problem up.

Chris says he gets up to 8 ounces of liver per week. That's up to 5mg of retinol per day just from liver. That's 15,000 IU. Then he takes some supplement on top "when he gets sick", plus eggs and dairy.

His daily intake probably approaches 20,000 IU, but could be easily 40,000 IU if he eats high carotene vegetables like spinach. Chris Masterjohn simply suffers from chronic vA toxicity and he rather extensively analyzes his genome and looks for fantasy diseases than confronting the simple truth.

 

[Nick]

Your first statement is not a rebuttle its an opinion, in particular the statement calling mutations of receptors "junk science". I think without further support or extension, this statement is largely irrelevant to the specific conversation at hand.

If receptors don't exist then by definition any experimenter that uses mutations of receptors does not actually understand what is actually happening in their experiment and no conclusions can be drawn from it. Ray Peat also did not think receptors exist. I'm not going to make the whole argument about the evidence for this here because it's simply too big an issue, how biology doesn't actually understand much of what it looks at under the microscope.

If you want to look into start here: https://raypeat.com/articles/articles/pdf/Estrogen-Receptors-what-do-they-explain.pdf

 

[CLASH]

That's why I suspect the "vitamin a depleted rats" in the steroidogenesis studies were actually the most toxic, and ascorbic acid acted protectively to prevent some of the consequences. Just as Grant Genereux always said.



The meta-analysis looks for people with clinical toxicity. To be included in such a meta-analysis, the vA toxicity must be extreme.

"... that the following serum markers were most commonly elevated: retinol in 89% of cases, γ-glutamyltranspeptidase in 83%, lipids in 80%, triglycerides in 75%, alkaline phosphatase in 67%, prothrombin time in 53%, cholesterol in 50%, aspartate aminotransferase in 49%, bilirubin in 48%, and calcium in 46%. "

Retinol is only elevated in extreme cases when the body can't regulate the homeostasis anymore.

When Grant Genereux, Dr. Smith and people here talk about vA toxicity, they are usually talking about "subclinical" toxicity that is not measurable with the usual blood tests (except some tests that are not commonly used, like free retinyl esters). In other words, medicine is just looking at the wrong parameters to define toxicity. As usual, they take the most obvious/extreme cases and then exclaim everything else does not exist.

People who get chronically depressed, have hair loss, anxiety, sleep problems, chronic fatigue, etc. etc. from RDA levels of retinol, but don't match the above blood parameters will never be grouped under the term "vitamin A toxicity", even though they get healthy from stopping the vA intake.

It's just the usual vodoo witchcraft of modern medicine. First, they define the problem in a way to distort the truth, and then they can tell people that nothing is there and they are just making their problem up.

Chris says he gets up to 8 ounces of liver per week. That's up to 5mg of retinol per day just from liver. That's 15,000 IU. Then he takes some supplement on top "when he gets sick", plus eggs and dairy.

His daily intake probably approaches 20,000 IU, but could be easily 40,000 IU if he eats high carotene vegetables like spinach. Chris Masterjohn simply suffers from chronic vA toxicity and he rather extensively analyzes his genome and looks for fantasy diseases than confronting the simple truth.

Suspecting a mechanism doesn't make it correct. It would be helpful for you to support your specific thoeries to make your point.

-----

This is the one of the glaring problems.

Since this "subclinical toxicity" can't be measured without obscure testing, a large theory has been created and hyped without specific verification.

The anecdotes being shared are nice in the sense that some people are feeling better, but these aren't specifically supportive of vitamin A being the issue, since in most cases no testing is being done and many things are being changed in conjunction with the lowering of vitamin A intake.

-----

People who get chronically depressed, have hair loss, anxiety, sleep problems, chronic fatigue, etc. can have a variety of underlying causes for these symptoms that aren't specific for vitamin A toxicity. Furthermore feeling a bit better when switching to the "low vitamin A diet" isn't proof that vitamin A was the cause of these problems. Multiple factors are being changed simultaneously besides just vitamin A with this diet.

-----

You dont think theres a hint of voodoo witchcraft in promoting the idea that most peoples issues are due to vitamin A toxicity, without actually directly testing this hypothesis?

-----

Did you read the meta analysis quote Chris shared? The threshold for toxicity of vitamin A with concurrent consumption of vitamin D3 is significantly higher than the estimated 40,000IU that you are proposing.

You are entitled to your opinions on Chris' health state, however your opinion on his health state isn't a rebuttle to the meta-analysis cited information.

-----

I'm open to the idea that the threshold for cumulative vitamin A toxicity is lower than traditionally understood, which is why I am reading Grant's work. However the information provided thus far on this forum isn't really that convincing for the theory. The arguments and evidence shared here are relatively weak and theres quite a bit of hype.

 

[CLASH]

If receptors don't exist then by definition any experimenter that uses mutations of receptors does not actually understand what is actually happening in their experiment and no conclusions can be drawn from it. Ray Peat also did not think receptors exist. I'm not going to make the whole argument about the evidence for this here because it's simply too big an issue, how biology doesn't actually understand much of what it looks at under the microscope.

If you want to look into start here: https://raypeat.com/articles/articles/pdf/Estrogen-Receptors-what-do-they-explain.pdf

The key statement in your response is "If receptors dont exist..."

You have yet to show evidence that receptors dont exist.

Also, its tenuous to say "no conclusions can be drawn from it". Even in the article you cited Ray was inferring information from receptor studies while he was questioning the usefulness of receptor ideology. For example:

"Although some of the experimental results are hard to relate to the supposed biological actions of the receptors, the alteration of these proteins by estrogen in a cold system is interesting in itself, since it indicates that estrogen changes the stability of the proteins when the watery solution is close to its freezing point, something which might be applicable to many other proteins and which could have important implications for receptor the way estrogen acts."

Lastly, Ray's article does not discount the existence of a protein response at the membrane (aka a receptor), he brings into question the centrality of the receptor in manifesting estrogen's effects. I would agree with Ray that the current ideology around receptors is likely too far in favor of reductionistic mechanisms (his ideas around the water destructuring effects of estrogen are extremely interesting), however I find it difficult to claim receptors dont exist at all and to imply that all research that uses them is "junk science".

 

[charlie]

I'm open to the idea that the threshold for cumulative vitamin A toxicity is lower than traditionally understood, which is why I am reading Grant's work. However the information provided thus far on this forum isn't really that convincing for the theory. The arguments and evidence shared here are relatively weak and theres quite a bit of hype.

Irreversible stage 4 kidney disease healed, irreversible cirrhosis of the liver gone, both doctors said they never have seen that before. At least two people with type 1 diabetes gone and off insulin. Countless other testimonies and healings across the board including my own miraculous turnaround. A family member who just started recently said they have had the most energy they had in they cannot remember how long. And this family members main complaint was energy. At least 4 people on the forum have already started to unlock their livers and well on the road to Restoration.

Convincing enough for me.

And yes, it has been tested, Dr. Garrett Smith who is in clinical practice is seeing this is real time. You are spreading bad information and it's not a good look on you, Clash.

Furthermore feeling a bit better

Hogwash. People are feeling better then they have in their entire lives. Your rhetoric is duly noted and your undertones will not last long around here.

You dont think theres a hint of voodoo witchcraft in promoting the idea that most peoples issues are due to vitamin A toxicity, without actually directly testing this hypothesis?

You are the one directly conjuring witchcraft with what you think are slick undertones. It wont work, Clash. Either hunker down and figure out how to help make this process better, or move on.

This new paradigm is simple ya'll. Some would have you believe achieving health is complicated so they can keep you in chains. We are being freed from those chains and the countless rabbit holes and nuances they keep you trapped in. Freedom is here.